. 2009 May 14;2(Suppl 2):138–176. doi: 10.1159/000213161
Obes Facts. 2009 May 14;2(Suppl 2):138.
Introduction
Sleep disordered breathing (SDB) is more prevalent in obese children and adolescents and it is an independent risk factor for the metabolic syndrome. Oxidative stress and inflammation are two of the possible linking mechanisms. In this study we assessed the effects of weight loss and residual SDB on oxidative stress and systemic inflammation.
Methods
Consecutive obese children between 10 and 18 years of age, admitted at the revalidation centre “Zeepreventorium”, were included. They followed a multi-component treatment program, including diet and physical activity. All subjects had a sleep screening and venous blood sample, before treatment and after 4 to 6 months of therapy.
Results
Mean nocturnal saturation (<SaO2>) correlated significantly with leukocyte counts, neutrophil levels and uric acid before therapy, after adjusting for obesity. Following weight loss treatment leukocyte counts, neutrophil levels and uric acid decreased. Subjects with residual SDB still showed higher levels of uric acid, reflecting oxidative stress. Lower leukocyte counts correlated with an improvement in <SaO2> in girls, not in boys. The change in neutrophil levels was mediated by a decrease in BMI z-score in girls. Age and a decrease in BMI z-score were significantly associated with improvements in uric acid.
Conclusion
The severity of SDB is independently associated with inflammatory markers and oxidative stress in obese children and adolescents. Subjects with residual SDB after weight loss have higher levels of uric acid, reflecting oxidative stress. A decrease in leukocyte count is mediated by an improvement of <SaO2>, but this effect is gender-specific.
Conflict of interest: None Disclosed. Funding: No Funding.
Obes Facts. 2009 May 14;2(Suppl 2):138.
Introduction
The epicardial adipose tissue, which surrounds the coronary arteries, is a novel depot whose products may affect vascular homeostasis. This study investigated epicardial adipokine secretion in obesity and CAD.
Methods
Epicardial and thoracic subcutaneous adipose tissue samples were obtained during cardiac surgery from Caucasian, non-diabetic patients, with (n=44) and without angiographically significant CAD (n=22); subdivided into normal-weight (BMI≤27 kg.m−2) and obese subgroups (BMI>27 kg.m−2). Adiponectin, leptin, IL-6 and RANTES levels were determined in serum and supernatant of 24h adipose organ cultures.
Results
Obese individuals, with or without CAD, showed comparably low epicardial adiponectin release; CAD attenuated this release only among normal-weight individuals [median (IQR), normal-weight/controls 111.5 (66.2-182.9) ng/g/h versus obese/controls 55.2 (38.1-105.5) ng/g/h, p=0.05 and versus normal-weight/CAD 44.7 (33.3-91.0) ng/g/h, p=0.007].
Epicardial RANTES was elevated in CAD [normal-weight/CAD 117.4 (98.0-273.0) pg/g/h versus normal-weight/controls 39.4 (32.6-46.5) pg/g/h, p=0.001 and versus obese/controls 53.7 (44.7-86.8) pg/g/h, p=0.01] and its release increased marginally only in obese subjects free of CAD (p=0.04).
When obesity and CAD were assessed as continuous variables (BMI/number of diseased vessels), epicardial adiponectin correlated with BMI (r= −0.25, p=0.03) and with severity of CAD only after controlling for BMI (r= −0.34, p=0.02). Conversely, epicardial RANTES correlated with severity of CAD, irrespective of BMI (r=0.46, p=0.007). Epicardial leptin and IL-6 release were unrelated to obesity and/or CAD.
Conclusions
Epicardial adipokine release is differentially modulated; with adiponectin related to obesity, RANTES to CAD and leptin and IL-6 of lesser direct relevance. Studies on the pathophysiological significance of these changes are warranted.
Conflict of interest: None Disclosed. Funding: Research relating to this abstract was funded by European Commission (LSHM-CT-2004-005272) and AOYS/St George's Charitable Foundation.
Obes Facts. 2009 May 14;2(Suppl 2):138.
Introduction
We investigated the regulation of adipose tissue (AT) gene expression during different phases of a dietary weight loss program and its relationship with insulin sensitivity (IS).
Methods
Obese women underwent a dietary intervention (DI) program composed of an energy restriction phase (ER) with a 4-week VLCD and a weight stabilization (WS) period with a 2-week LCD and 3-4 months of a weight maintenance diet. Before DI and at the end of each phase, anthropometric and plasma parameters were assessed and euglycemic hyperinsulinemic clamp and subcutaneous AT biopsies were performed. Variations in mRNA levels were determined using DNA microarrays and RT-qPCR. Gene expression of 31 human AT macrophage-specific markers was also measured.
Results
Body weight and fat mass decreased and IS increased during the ER and WS phases. Two main patterns of variations in gene expression were observed. The first was composed of 464 genes downregulated during ER, upregulated during WS and unchanged during DI. The genes were mostly adipocyte genes involved in metabolism. The second comprised 511 genes not or upregulated during ER and downregulated during WS and DI. The genes were mostly macrophage genes involved in inflammatory pathways. Indeed, macrophage-specific markers were upregulated during ER and downregulated during WS and DI. Genes explaining changes in IS were different between ER and DI.
Conclusion
During different phases of a DI, distinct sets of AT genes are regulated and difference in macrophage gene expression is seen revealing an unexpected temporal pattern in the link between AT and IS during a weight loss program.
Conflict of interest: None disclosed. Funding: Inserm, grants IGA NR 9161-3-2007, GA R 303/07/0840 & MSM 0021620814, Midi-Pyrénées Region and EC Projects HEPADIP and ADAPT
Obes Facts. 2009 May 14;2(Suppl 2):139.
Introduction
Epicardial visceral fat (EAT), accumulated around the heart, is considered an index of visceral adiposity and a promising indicator of high cardio-metabolic risk. Evidences showing that EAT is a metabolically active organ and source of several inflammatory adipo-chemo-cytokines, suggest a condition of chronic inflammation in this small cardiac fat depot. However, the potential links between cardiac adiposity and circulating levels of inflammatory adipo-chemokines, as markers of suclinical inflammation, are not completely understood. This study was aimed to evaluate whether cardiac adiposity, measured as echocardiographic EAT thickness, is related to Regulated on activation, Normal T Cell Expressed and Secreted (RANTES/CCL5) plasma levels, in patients with uncomplicated obesity.
Methods
EAT thickness (measured by echocardiography), RANTES/CCL5 and some inflammatory markers were studied in 36 women affected by uncomplicated obesity (OB) (BMI 41.6±5.6 kg/m2) and 15 normal-weight controls. Abdominal visceral adipose tissue (VAT) in the OB was assessed by computed tomography.
Results
OB had thicker EAT (p<0.0001) and higher RANTES/CCL5 (p<0.03) concentrations than controls. EAT thickness and Log-RANTES/CCL5 concentrations directly correlated with indices of fat distribution (VAT, VAT/subcutaneusAT and waist, p<0.001). In multiple regression analysis log-RANTES/CCL5 most correlated with EAT thickness (T=3.93) and VAT (T=3.77), the others indices of fat distribution did not enter the model.
Conclusions
a) EAT thickness, an indicator of cardiac adiposity, may be significantly related to inflammatory adipo-chemokines in visceral-obese patients; b) this suggests that EAT thickness might be used in such patients as a reliable marker of visceral adiposity and subclinical inflammation, all preconditions to cardio-metabolic disorder.
Conflict of interest: None Disclosed. Funding: No Founding
Obes Facts. 2009 May 14;2(Suppl 2):139.
Introduction
Obesity is characterized by a systemic mild inflammatory state. In this context, TNF-alpha is a proinflammatory cytokine elevated in adipose tissue of obese subjects, whose promoter is susceptible to be regulated by cytosine methylation, an epigenetic process. The aim of this research was to analyze whether methylation of human TNF-alpha promoter could be considered as a biomarker of the predisposition to lose body weight after following a balanced hypocaloric diet.
Methods
Twenty-four patients (12 women and 12 men) with excess body weight (BMI: 30.5±0.32 kg/m2), followed an 8-week energy-restricted diet. Blood mononuclear cell DNA, isolated before the nutritional intervention, was treated with bisulfite, and a selected region of TNF-alpha gene promoter (from −360bp to +50bp) was sequenced.
Results
Obese men with successful weight loss (≥5% of initial body weight) showed lower levels of total TNF-alpha promoter methylation (r = 0.74; p = 0.021), specially in the positions −170bp (r = 0.75, p = 0,005) and −120bp (r = 0.70, p = 0.011). Baseline TNF-alpha circulating levels were positively associated with total promoter methylation (r = 0.84, p = 0.005) and the methylation at position −245bp (r = 0.75, p = 0.020). Also, endpoint TNF-alpha circulating levels correlated positively with the methylation levels of the promoter at position −245bp (r = 0.767, p=0.016).
Conclusion
TNF-alpha promoter methylation could be a good inflammation marker predicting the hypocaloric diet-induced weight-loss, and a first step towards personalized nutrition based on epigenetic criteria.
Conflict of Interest: None Disclosed. Funding: Research relating to this abstract was funded by the Linea Especial about Nutrition, Obesity and Health from University of Navarra (LE/97), the Basque Government's Department of Education, Universities and Research, and the Department of Education of the Government of Navarra.
Obes Facts. 2009 May 14;2(Suppl 2):139.
Introduction
We aimed to assess the relationship between inflammatory mediators and categories of glucose tolerance and obesity, and changes in these mediators after an oral glucose load.
Methods
Osteoprotegerin (OPG), visfatin, leptin, adiponectin, interleukin-1 receptor antagonist (IL-1Ra) and C-reactive protein (CRP) were analyzed before and during an oral glucose tolerance test (OGTT) in144 morbidly obese subjects classified as having; normal glucose tolerance (NGT), pre-diabetes and new onset diabetes, and in 27 normal weight, normoglycemic controls.
Results
Fasting serum levels of leptin and IL-1Ra were consistently higher in obese persons (p<0.001 and p=0.002, respectively), but did not differ between glucose tolerance categories. On the other hand, the levels of CRP increased and adiponectin decreased both with obesity and with advancing impairment of glucose tolerance (both p<0.001). There was no difference in baseline OPG and visfatin levels between the groups. OPG levels decreased (p<0.001) and visfatin levels increased transiently (p=0.018) during the OGTT, independent of obesity and glucose tolerance status. In contrast, there were no (IL-Ra and CRP) or only minor (adiponectin and leptin) changes in the other parameters during the OGTT.
Conclusions
Fasting serum levels of CRP were gradually elevated and adiponectin levels gradually reduced across various categories of glucose tolerance, supporting a relationship between inflammation and glucose intolerance in morbidly obese subjects. In addition, OPG levels decreased and visfatin levels transiently increased during the OGTT, indicating that glucose may be involved in the acute regulation of these proteins.
Conflict of Interest: None disclosed. Funding: Dag Hofs⊘ has received unrestricted educational grants from Novo Nordisk A/S, South-Eastern Norway Regional Health Authority and Vestfold Hospital Trust.
Obes Facts. 2009 May 14;2(Suppl 2):140.
withdrawn
Obes Facts. 2009 May 14;2(Suppl 2):140.
Introduction
During the past years, there has been a dramatic increase in the prevalence of obesity in developed nations. Recent studies indicate that adipose tissue is an endocrine organ producing numerous proteins, These adipokines with broad biological activity, have influence on other cytokines responsible for inflammation, and play an important autocrine role in obesity-associated complications.
Methods
In our study we analyzed changes in some cytokines plasma levels and their soluble receptors in severe obese patients undergoing bariatric surgery. Comparison enclosed results of 54 patients selected for bariatric surgery - mean body weight 132.6 kg, mean BMI 45.6 kg, mean body fat 47.4%, mean age 39,4 years old, 38 women, 16 men. Using Enzyme-Linked Immunosorbent Assay (ELISA) we determined plasma levels of interleukin-6 (IL-6), leptin, adiponectin, TNF-α and soluble receptors for IL-6 (IL-6sR) and TNF-α type I and II (sTNF RI and sTNF RII) before and 12 months after surgery. We also analyzed if type of surgery had an impact on changes in cytokines activity.
Results
42 patients (mean BMI of 46.3 kg/m2, mean body fat of 47.1%, mean age 41,4 y/o, 26 women) underwent open Vertical Banded Gastroplasty (VBG) and 12 (mean BMI of 44.6 kg/m2, mean body fat of 48.4%, mean age 32,4 y/o, only women) open Roux-en-Y Gastric Bypass (RYGB). Comparing laboratory date assessed before and one year after surgery we found significant changes in plasma levels of IL-6 (2.41 vs 0.69 pg/ml; p<0.00001), leptin (44.49 vs 15.11 ng/ml; p<0.00001), sTNF RI (1.81 vs 1.41 ng/ml, p<0.00001), sTNF RII (3.22 vs 2.71 ng/ml; p<0.0001), adiponectin (5.02 vs 11.63 µg/ml, p<0.00001). We also noticed not significant lowering of TNF-α (2.30 vs 2.20 pg/ml) and IL-6sR (51.24 vs 49.63 ng/ml) levels. Type of surgery had no impact on this changes
Conclusion
Weight loss after bariatric surgery is accompanied by an decrease in circulating concentrations of the proinflamatory cytokines. This decrease strongly correlates with the increase in plasma adiponectin concentrations. Type of surgery had no impact on this changes.
Conflict of Interest: None Disclosed. Funding: Research relating to this abstract was partially funded by Polish Ministry of Science and Higher Education, grant number N 403 041 31 / 2301
Obes Facts. 2009 May 14;2(Suppl 2):140.
Introduction
Obesity is associated with vascular dysfunction as well as an increase in the prevalence of retinopathy and microvascular retinal alterations. However, it is not known whether there are early signs of macular oedema, a microvascular complication of the macular, in obese individuals.
Aims
1) determine whether obesity alters microvascular determinants of fluid filtration, microvascular resistance, or markers of systemic inflammation, 2) explore whether alterations in these parameters are reflected in macular thickness (oedema).
Method
In 21 obese (BMI>29) and 21 age, sex matched lean (BMI<25) subjects, fovea thickness, capillary pressure (CP), microvascular filtration capacity (Kf), minimum vascular resistance (MVR) and inflammatory markers (eg C-reactive protein, CRP) were measured.
Results
Elevated CP and MVR were observed in the obese group (CP: obese, geometric mean: 16.7(confidence intervals: 15.5,22.3) vs lean: 14.0(12.0,17.1)mmHg, p=0.005 t-test); MVR obese: 55(47,65) versus lean: 41(35,50)mmHg / volts, p=0.012). Kf was lower in the obese subjects (obese mean: 3.21(SD:1.04) versus lean: 4.02(0.85)KFU, p=0.012). Fovea thickness did not differ between groups (obese 212.3(22.6) vs lean 216.0(20.4)µm, p=0.613). Extending the subject group (n=50) to create a continuum of BMIs (20.0-46.3), CP was positively associated with fovea thickness (R2=0.144,p=0.027, linear regression). Insulin sensitivity was lower and HbA1c and CRP were higher in obese compared to lean subjects.
Discussion
Impairments in microvascular function occur in obese subjects: raised CP and MVR and reduced Kf, suggesting microvascular rarefaction. However, these alterations were not reflected by alterations in macular thickness.
Conflict of Interest: None Disclosed. Funding: Research relating to this abstract was funded by Diabetes UK
Obes Facts. 2009 May 14;2(Suppl 2):140.
Introduction
Our objective was to examine if a combination of high-protein and low-carbohydrate intake (HPLC) compared to high-protein (HPNC) or low-carbohydrate (NPLC) or normal-protein normal-carbohydrate intake (NPNC) results into a difference in weight loss and body-composition.
Methods
Body-weight and body-composition (deuterium-dilution-technique) of 143 subjects (BM 106.6±20.1kg and FM% 43.9±5.8%) and blood- and urine-parameters were assessed before and after a 3-months energy intake reduction of 67%. The HPLC-diet consisted of 60/5/35E% protein/carbohydrate/fat and resulted in 120±41g of protein intake (24-hour nitrogen), HPNC of 60/35/5E% and 105±30g, NPLC of 30/5/65E% and 73±21g, and NPNC of 30/35/35E% and 67±16g.
Results
The HPLC-diet was the most effective in reducing BM and FM%. The synergistic effect of HP and LC and the effect of HP in the LC condition was already significant on BM-reduction after 1-month (HPLC vs. NPNC −6.7±2.1vs.-5.1±1.8, p<0.005; and vs. NPLC −5.8±1.7, p<0.05). The effect of HP was significant in the normal- (3-months delta HPNC vs. NPNC; BM −12.6±4.1vs.-10.6±4.0, p<0.01 and FM% −5.7±3.3vs.-3.9±2.5, p<0.05) and the low-carbohydrate condition (3-months delta HPLC vs. NPLC; BM −15.3±4.5vs.-12.2±4.4, p<0.01 and FM% −6.6±2.6vs.-4.8±3.7, p<0.05). There was no effect of LC in the normal- (NPLC vs. NPNC) or the high-protein (HPLC vs. HPNC) condition. Changes in waist-circumference, waist-hip-ratio, MDRD, urine albumin-creatinin-ratio, glucose, insulin, HOMA, and HDL-, LDL-, total-cholesterol and total-HDL-ratio were not different between diets.
Conclusion
High-protein shows a larger decrease in BM and FM% irrespective of the presence of low-carbohydrate, while low-carbohydrate only shows a larger decrease in BM and FM% in the presence of high-protein.
Conflict of Interest: None Disclosed. Funding: No Funding
Obes Facts. 2009 May 14;2(Suppl 2):141.
Objective
Beneficial effects of low glycemic index (GI) diets in rodents have been studied using healthy low fat diets, while the effects might be different on high fat diets inducing progression of insulin resistance.
Methods
C57BL/6J adult male mice were fed high-fat low/high GI (LGI/HGI) diets for 13 weeks. Glucose and insulin tolerance and serum substrates, including adipokines, were measured longitudinally. Adipose tissue expression of adipokine genes was analyzed by Q-PCR.
Results
Food intake was similar throughout the study, but body weights and epididymal adipose tissue mass were significantly lower in the LGI group after 13 weeks. A significant higher glucose tolerance in the LGI group was observed from week 2 onwards, which was supported by lower serum insulin and free fatty acids levels at 8 weeks, a tendency for lower leptin levels, while resistin and PAI-1 levels remained similar. At 11 weeks, when differences in serum resistin started to increase, differences in serum insulin were diminished. Several serum substrates and adipose tissue leptin mRNA levels were (again) significantly lower after 13 weeks in the LGI group, while adiponectin mRNA levels were higher.
Conclusion
Although a LGI diet is not able to arrest high fat diet-induced development of insulin resistance, higher glucose tolerance and insulin sensitivity is observed from week 2 onwards until section in week 13. This retardation is solely caused by a difference in the type of carbohydrate of the diet, supporting a nutritional approach in the fight of insulin resistance.
Research relating to this abstract was funded by Top Institute of Food and Nutrition, Wageningen, The Netherlands
Obes Facts. 2009 May 14;2(Suppl 2):141.
Introduction
Human eating behaviour can be influenced non-homeostatically by the rewarding value of foods, i.e. liking and wanting. The aim of this study was to determine how the rewarding value of food is affected by eating dessert-specific (chocolate mousse, CM) vs. dessert non-specific food (cottage cheese, CC) in normal-weight dietary-unrestrained(NU)/ restrained(NR) and visceral-overweight(VO) subjects.
Methods
Subjects (25 NU, age=25.1±8.1yrs, BMI=22.2±1.7kg/m2; 24 NR, age=25.0±8.2yrs, BMI=22.3±2.1kg/m2, factor 1 from the Three Factor Eating Questionnaire=11.8±2.2; 21 VO, age=35.4±10.9yrs, BMI=28.5±1.5kg/m2, waist/hip=0.9±0.1), studied in a randomized cross-over design, came to the university twice in a fasted condition. They completed a liking and wanting-test for 72 items divided in 6 categories (bread, filling, drinks, dessert, sweets, stationery), before and after consumption of CM or CC, matched for energy content (5.6kJ/g) and daily energy-requirements (10%).
Results
CM was liked more than CC (p<0.01). In NR a decrease in wanting for bread, filling, drinks and dessert (p<0.02) was observed after CM-consumption and for drinks and dessert (p<0.03) after CC-consumption. In NU and VO wanting for different categories did not change after CM/CC-consumption. Ranking of liking showed a decrease of the dessert-category (p<0.004) and an increase of the stationery-category (p<0.0006), after CM-consumption. CC induced an increase in the ranking of liking of stationery (p<0.0005) in NU and NR, and of sweets in VO (p=0.02).
Conclusion
Eating a dessert-specific food item decreases wanting for food more than eating a less liked dessert non-specific food item only in normal-weight dietary-restrained subjects, and induces a lower ranking of category-specific liking in normal-weight dietary-unrestrained, restrained and visceral-overweight subjects.
Conflict of Interest: None Disclosed. Funding: Research relating to this abstract was funded by Top Institute Food and Nutrition
Obes Facts. 2009 May 14;2(Suppl 2):141.
Introduction
Concurrent with the obesity epidemic, numerous epidemiologic studies reported a parallel epidemic of chronic sleep deprivation. No experimental study reported caloric intake and physical activity after acute sleep deprivation in humans.
Methods
12 male normal-weight volunteers (22±3 yr, BMI: 22.3±1.8) were evaluated in two 48h-randomized sessions. During the first night of each session, subjects had either ~8 hrs (from midnight to 8 a.m.) or ~4 hrs (from 2 a.m. to 6 a.m.) of sleep. All foods consumed subsequently (jam-buttered toasts for the breakfast, buffet for the lunch and free menu for the dinner) were eaten ad libitum. Physical activity was registered by an actimeter. Hunger and sleepiness sensations, pleasantness of the foods, liking/wanting for some food items, were also evaluated.
Results
Subjects ate 559±617 kcal [3456±3819 kJ] (i.e. 22%) more energy the day after the deprived sleep in comparison to the normal sleep (p<0.01) with hunger sensation higher before the breakfast and the dinner (p<0.05). Pleasantness induced by the foods as well as liking/wanting for the food items did not differ between the two sessions. Physical activity was 17% higher the day after the deprived sleep in comparison to the normal sleep (p<0.01), albeit sleepiness sensation was higher after the deprived sleep (p<0.01).
Conclusion
These results indicate that sleep deprivation increases food intake and to a lesser extend physical activity in the short term. With epidemiologic studies, these results show that sleep deprivation could be a factor promoting obesity.
Obes Facts. 2009 May 14;2(Suppl 2):141–142.
Introduction
Fat oxidation has been implicated in the energostatic control of eating and may provide a metabolic stimulus for energy intake (EI). The objective of this study was to examine the relationship between substrate oxidation during exercise and the variability in EI compensation following medium-term exercise training.
Methods
Thirteen overweight and obese men (n=5) and women (n=8) with a mean BMI=30.6±4.5kg/m2, age=43±6.4yrs and VO2max=30.0±6.5ml·kg·min−1 completed 8 weeks of supervised aerobic exercise. At weeks 0 and 8 the non-protein respiratory exchange ratio (RER) was measured (cycling, 60mins, 70%HRmax) and measures of body composition and EI (test meals) were taken.
Results
Following the exercise intervention body weight, fat mass and percentage body fat decreased by −1.8±2.0kg (t=3.20, p<0.00), −2.7±1.5kg (t=7.4, p<0.00) and −2.2±1.1% (t=6.01, p<0.00), respectively. While mean EI did not change between weeks 0-8 (t=1.11, p=0.28), large inter-individual variation was observed (change in EI ranged from −482kcal/day to +550kcal/day). Exercise RER decreased from 0.86±0.03 to 0.83±0.04 (t=2.37, p=0.03), equating to a 10.3% reduction in the percentage of energy derived from carbohydrate and an equivalent increase in fat utilization. Exercise RER and the rate of fat oxidation at week 0 were correlated with the change in EI (r=0.70, p<0.00; r= −0.83, p<0.00, respectively) and fat intake (r=0.41, p=0.04; r= −0.52, p=0.06, respectively) between weeks 0-8.
Conclusion
These data indicate that EI compensation to medium term exercise training is highly variable, and those who demonstrate attenuated fat utilization during exercise at the start of training display greater EI compensation at the end of exercise training.
This project was funded by the Biotechnology and Biological Sciences Research Council (BBS/B/05079).
Obes Facts. 2009 May 14;2(Suppl 2):142.
Introduction
People who eat more dietary fiber have a lower body weight than people who eat less fiber. Potential mechanisms include greater feelings of satiety, reduction in food intake, changes in blood glucose, insulin, or gut hormones. We hypothesize that different doses of a mixed fiber supplement will influence satiety response and food intake when given to subjects in muffins for breakfast.
Methods
Healthy men (n = 10) and women (n = 10) with a body mass index of 23.7±0.5 (mean±SEM) participated in this randomized double-blind, crossover study. On four separate visits, fasting subjects consumed a muffin with 0, 4, 8, or 12g of mixed fibers. Muffins had 500 calories and similar macronutrient content. Visual analogue scales rated hunger and satiety from 0-180 minutes; blood was drawn to measure glucose, insulin, and gut hormones (ghrelin, PYY 3-36, GLP-1). Food intake at lunch was measured 180 minutes after muffin consumption.
Results
In all satiety measures, 12g muffins were significantly different from 0g muffins. Muffins with 4g and 8g of fiber were intermediate. Despite differences in satiety measures after three hours, food intake was not different among treatments. Glucose, insulin and GLP-1 response did not correlate with fiber dose. Ghrelin was significantly higher after 12g of fiber. There were no differences in PYY.
Conclusion
Feelings of hunger, satisfaction, fullness, and desire to eat differ after consuming 0, 4, 8, or 12g of mixed fiber for breakfast, but were not consistently linked to physiologic measures or food intake.
Conflict of Interest: None Disclosed. Funding: Funding received from Nestle Research Center, Lausanne, Switzerland
Obes Facts. 2009 May 14;2(Suppl 2):142.
Introduction
Satiation is the process that brings a meal to an end. In terms of preventing over consumption, it is of great importance to identify features of foods that influence this process. Sensory properties have been shown to play a major role. The objective of this study was to investigate the difference between a distinct sweet and savory taste on satiation, independent of palatability, texture, energy density and macronutrient composition.
Methods
A cross-over design consisting of three test-conditions in which two tastes (sweet and savory) were compared. Sixty-four healthy, nonsmoking, unrestrained subjects participated (18 males and 46 females), with a mean age of 22.3 years (SD 2.4) and a mean BMI of 21.6 kg/m2 (SD 1.7). Rice was used as a test food, served in either a sweet or savory variant. The meals were similar in palatability, texture, energy density and macronutrient composition. Ad libitum intake, eating rate and processes of appetite and pleasantness during the meal were measured.
Results
No differences were found in ad libitum intake between the two meals. Subjects ate a mean of 314.2 g of the sweet rice and 333.4 g of the savory rice [t(64) = −1.18, n.s.]. In addition, the eating rate (sweet: 37.7 g/min; savory: 36.6 g/m [t(64) = 0.79, n.s.]) and the changes of appetite and pleasantness during the meals were equal.
Conclusion
Meals with a sweet or savory taste, similar in palatability, texture, energy density and macronutrient composition, do not differ in their influence on satiation in normal weight people.
Obes Facts. 2009 May 14;2(Suppl 2):142.
Introduction
Small fat droplets infused into the small intestine reduce food intake and hunger more than bigger ones. It is not known if these effects are relevant when the fat is consumed orally, or at what amounts of fat. We therefore tested the effect of fat droplet size (3 versus 0.1 micron) of different amounts of fat (5g versus 9g) in a drink on satiety, food intake and cholecystokinin (CCK).
Methods
In a balanced order 4-way cross-over design, 24 volunteers (8 male, mean age 46y, BMI 24 kg/m2) consumed a fat-free Slim-Fast meal replacement drink at t=0 min with either 5g or 9g oil and either 3 or 0.1 micron droplet size. Appetite scores and plasma CCK levels (in n=12 subset) were measured for 180 min, when food intake was assessed during an ad libitum meal. Data were analyzed by ANCOVA, followed by Dunnett. The behaviour of the emulsions was also characterized in a simulated gastro-intestinal model.
Results
Surface-weighted mean diameter of fat droplets in the simulated stomach increased slightly (from 3 to 5 and from 0.1 to 0.2 micron). Despite faster in vitro lipolysis of the 0.1 micron droplets, neither droplet size nor fat amount affected satiety or food intake. From t=45-150 min CCK response was 50% higher (P<0.05) after the 0.1 versus 3 micron, but only with 9g fat.
Conclusions
When fat was delivered in a drink, droplet size did not influence appetite or food intake, independent of the amount of fat or plasma CCK changes.
Funding/Conflict of Interest: Research was funded by Unilever, a commercial manufacturer of meal replacer.
Obes Facts. 2009 May 14;2(Suppl 2):143.
Introduction
A causal link has been suggested between meal-induced thermogenesis and satiety. This has been explained by observation that protein is known to stimulate both thermogenesis and satiety. The objective of this individual participant data (IPD) meta-analysis was to test the association between appetite sensation and meal-induced thermogenesis (MIT).
Methods
We conducted an IPD meta-analysis on studies previously performed at Department of Human Nutrition, University of Copenhagen, Denmark. The included studies were all randomized trials testing different types of meals in respiration chambers. Furthermore, the studies measured appetite sensations using Visual Analogue Scales (VAS).
Results
Five randomized meal-test trials (with a total of 111 subjects) were included. The IPD meta-analysis showed no association between satiety and MIT (P=0.48). Likewise, neither the average VAS score (composite VAS), fullness, prospective food intake or hunger were associated with MIT (p>0.65). The analysis showed no association between MIT and amount of protein intake (P=0.7). Finally, no association between satiety and protein intake (P=0.59) or between composite VAS and protein intake was observed (P=0.54).
Conclusions
Our results suggest that there is no association between satiety or the average appetite score (composite VAS) and meal-induced thermogenesis at moderate protein intakes ~15 E% (range 11-30 E%). Furthermore, we found no association between fullness, prospective food intake or hunger and meal-induced thermogenesis. Further studies are needed to clarify whether the previously suggested association between satiety and meal-induced thermogenesis is truly causal.
Conflict of interest: None Disclosed. Funding: This research was supported by EC FP6 Diabesity project (LSHM-CT-2003-503041).
Obes Facts. 2009 May 14;2(Suppl 2):143.
Introduction
Oleoyl-estrone (OE) induces the loss of body fat by decreasing food intake and maintaining energy expenditure. WAT size, cellularity and lipid metabolism gene expressions were analyzed in different localizations to better understand how OE elicits the loss of lipids.
Methods
Male Wistar rats, made overweight by transient cafeteria dietfeeding were used. Treated rats received a daily gavage of 10 nmol/gBW OE during 10 days; controls and pair-fed received only the vehicle. The pair-fed rats were fed only the mean food consumed by the OE-treated rats. Mesenteric, perigonadal, retroperitoneal and subcutaneous inguinal fat pads were dissected, weighed and later used for the estimation of DNA and analysis of gene expression by a semiquantitative RT-PCR method.
Results
WAT weight of OE and pair-fed rats decreased in size but with limited loss of cells. The expression of lipogenesis-related genes (Acly, Fasn, Gpam, Adpn and Srebp-1c) diminished in OE-treated and pair-fed in all WAT sites, except in mesenteric (increased in pair-fed and unchanged in OE).
Conclusion
Patterns of gene expression in most WAT sites were similar for pair-fed and OE suggesting a shared mechanism of fat mobilization. The OE effects on WAT may be more a consequence of inhibited lipogenesis than enhanced lipolysis, an effect fully comparable to that induced by pair-feeding. Mesenteric WAT (i.e. a truly visceral WAT site) patterns were fairly different from the other depots.
Conflict of interest: None Disclosed. Funding: Grant SAF2006-05134 of Governament of Spain. And CIBER Obenutr, a ISCIII initiative.
Obes Facts. 2009 May 14;2(Suppl 2):143.
Introduction
NAFLD and the Metabolic Syndrome seem to be intimately linked. Studies suffer from selection bias or diagnostic inaccuracy. The physiopathology remains poorly understood. We studied in a prospective cohort of overweight patients the relationship between the metabolic syndrome and liver involvement, with emphasis on liver histology and haemodynamics.
Methods
Patients presenting to the obesity clinic underwent a metabolic and a detailed liver assessment. If liver involvement was suspected, liver biopsy was proposed, preferentially through a transjugular approach.
Results
55 patients underwent a transjugular biopsy (september 2006-may 2008), with mean age 45.5±14.9 y, mean BMI 40.4±7.2 kg/m2; 34 female (62%); 63% fulfilled the criteria of the MS. Thirteen (34%) had no steatosis, 4 (10%) had severe (>66%) steatosis; 7 (17%) met the criteria of NASH. Advanced fibrosis was present in 5 (12%). Fifteen (27%) had portal hypertension (PHT), indicating serious liver blood flow impairment. PHT was not related to fibrosis. Comparing those with and without PHT, only steatosis(p=0.013), waist(p=0.005), WHR(p=0.003), visceral fat(p=0.022), fasting insulin/c-peptide and HOMA IR(p=0.019) were significantly different. PHT was significantly correlated to steatosi s(r=0.38,p=0.012), waist(r=0.37,p=0.005), WHR(r=0.39,p=0.003), fasting c-peptide(r=0.36,p=0.026) and HOMA IR(r=0.32,p=0.019). The degree of steatosis was significantly correlated to waist(r=0.46,p=0.002), fasting c-peptide(r=0.45,p=0.003) and HOMA IR(r=0.50,p=0.001). After correction for waist, HOMA-IR(r=0.41,p=0.009) remained significantly correlated to steatosis.
Conclusion
In this unselected cohort of overweight patients, visceral fat and insulin resistance are independently correlated to steatosis, and these 3 elements are associated with fibrosis-independent PHT which might significantly contribute to their interaction.
Conflict of interest: None disclosed. Funding: This work is part of the project “Hepatic and adipose tissue and functions in the metabolic syndrome” (HEPADIP), which is supported by the European Commission as an Integrated Project under the 6th Framework Programme (Contract LSHM-CT-2005-018734).
Obes Facts. 2009 May 14;2(Suppl 2):144.
Introduction
Some investigators have advocated the use of sex hormone binding globulin (SHBG) as a predictive marker of insulin resistance (IR) in women with hyperandrogenism.
Objectives
To determine IR in obese hyperandrogenic women and to evaluate whether SHBG, free androgen index (FAI) and body mass index (BMI) are correlated to IR index.
Methods
The authors present a retrospective analysis of 126 obese women with elevated plasma androgen levels evaluated in the obesity outpatient clinic of Hospital São João. Anthropometric variables, plasma androgen and sex hormone binding globulin (SHBG) concentrations were measured. Insulin resistance was evaluated by the following index: homeostasis model assessment of insulin resistance (HOMA-IR), quantitative insulin sensitivity check index (QUICKI) and insulin sensitivity index-Matsuda (MATSUDA). It was defined by HOMA-IR≥2.5, QUICKI≤0.33 or MATSYDA≤5. Pearson's correlation coefficient and Student's t-test were used for the statistical analysis.
Results
Patients had mean age of 41.8±11.7 years and mean BMI of 41.1±7.4Kg/m2. 68.1% of these women had IR. Women classified as having IR had a significantly higher BMI and free androgen index (FAI) and significantly lower SHBG levels. BMI was negatively correlated with SHBG (r= −0.38; p<0.0001). FAI was positively correlated with HOMA-IR (r=0.32; p<0.003), QUICKI (r= −0.23; p<0.03) and Matsuda (r= −0.21; p<0.05). SHBG was negatively correlated with HOMA-IR (r= −0.25; p<0.007).
Conclusion
This study suggests that SHBG may serve as a predictive marker of IR in obese hyperandrogenic women.
Obes Facts. 2009 May 14;2(Suppl 2):144.
Introduction
Obesity increases the risk of diabetes. The aim of the study was to evaluate insulin resistance (IR) and impaired beta-cell function in obese patients with and without diabetes.
Methods
The study included 21 obese non-diabetic patients (age − 46.5±10.1 years, 8 men, BMI − 37.54±6.12 kg/m2, waist − 106.17±13 cm) and 19 obese diabetic patients (age − 55.33±4.44 years, 7 men, BMI − 35.71±2.9 kg/m2, waist − 102.5±11.3 cm, HbA1c − 7.77±1.13%, duration of diabetes − 1.8±0.8 years). Diabetic subjects were only on diet. The study groups were similar in terms of age, sex distribution, waist circumference, BMI. OGTT with 75 g of glucose was performed in all subjects. Glucose (mmol/l) and insulin (µU/ml) levels were determined from blood samples taken at 0, 30 and 120 minutes. IR was calculated using HOMA-IR index and first phase insulin response was estimated using insulinogenic index (IGI) at 30 minute (I30 - I0/G30-G0). For statistical analisys was used Student's t-test. P < 0.05 was considered statistically significant.
Results
In the non-diabetic group 10 (48%) subjects had normoglycemia (NGT), 5 (24%) subjects impaired fasting glucose (IFG) and 6 (28%) impaired glucose tolerance (IGT). There was no difference between obese non-diabetic patients and obese diabetic patients in HOMA-IR (4.2±2.24 vs. 5.48±2.48, p < 0.05) and fasting insulin (14.89±6.9 µU/ml vs. 13.26±5.47 µU/ml, p < 0.05). Beta cell secretion deteriorated significant in obese diabetic patients comparing with obese non-diabetic patients (IGI: 11.13±6 vs. 23.12±5.71, p=0.02; 120 minutes insulin level: 77.36±15.17 µU/ml vs. 166.7±79.67 µU/ml, p=0.047). In the non-diabetic study group there were no statistical differences in HOMA-IR and IGI between NGT subjects and subjects with IFG and IGT.
Conclusion
Beta-cell dysfunction has the main role in the progress of obese patients to diabetes.
Obes Facts. 2009 May 14;2(Suppl 2):144.
Introduction
Stunting is the best indicator for chronic nutritional deficit. The long-term effects of stunting include metabolic alterations that can result in non-communicable illnesses. However, few studies have investigated the presence of such alterations in stunted adolescents.
Methods
Was selected 268 boys and girls aged 9 to 18, residents of slums in São Paulo, Brazil (119 were stunted and 149 had normal stature). For each individuals, glucose, insulin and lipid profile were determined. Pancreatic b-cell function and insulin resistance were calculated according to the homeostatic model assessment (HOMA B and IR).
Results
Stunted individuals have statistically higher total cholesterol, levels of insulin, HOMA-IR and HOMA-B than for those classified as normal stature. The results were adjusted for gender, BMI and pubertal stage.
Conclusion
The present investigation revealed a significant association between stunting, dislipidemies and insulin alterarions. The present findings may be involved in the metabolic changes that are responsible for occurrence of higher prevalence of chronic diseases in adult life, such as obesity and type 2 diabetes, among stunted individuals.
Conflict of Interest: None Disclosed. Funding: Research relating to this abstract was funded by Fundação de Amparo a Pesquisa de São Paulo (FAPESP) and International Atomic Energy Agency (IAEA).
Obes Facts. 2009 May 14;2(Suppl 2):144–145.
Introduction
High fat diets rich in saturated fat are commonly used to generate obese and insulin resistant mouse models. However, relatively little is known about the role of specific saturated fatty acids (FA) in the development of pathology. Here, we have studied the role of specific FA on tissue specific insulin sensitivity and whole body energy metabolism.
Methods
C57Bl/6 mice were fed diets based on palm oil (HFP) and lard (HFL) or palm oil. Since the level of the saturated FA stearate (C18:0) is strikingly different, we also used a HFP diet supplemented with tristearin (HFP+S) to the level present in HFL. Tissue specific insulin resistance was determined by hyperinsulinemic-euglycemic clamp analysis. Whole body metabolism was assessed by indirect calorimetry employing metabolic cages.
Results
Clamp analysis revealed significantly lower insulin mediated repression of endogenous glucose production in mice fed the HFL and HFP+S diets. In contrast, insulin stimulated glucose disposal was higher in mice fed HFL and HFP+S diets. Metabolic cage analysis revealed higher food intake, lower caloric energy expenditure and a preferential oxidation of carbohydrates over fatty acids in lard fed animals compared to palm oil. Dietary tristearin supplementation resulted in lower caloric energy expenditure and preferential oxidation of carbohydrates versus fatty acids compared to palm oil. DEXA scan analysis revealed a higher fat to lean mass ratio in animals fed a stearate rich diet.
Conclusion
Elevated levels of dietary stearate result in increased hepatic insulin resistance and an adverse metabolic phenotype characterized by low levels of fat oxidation and accumulation of adipose tissue mass.
Obes Facts. 2009 May 14;2(Suppl 2):145.
Introduction
The ability to switch from fat to glucose oxidation upon insulin stimulation is termed metabolic flexibility and is hypothesized to play a role in the development of obesity and insulin resistance. Here, we set out to determine (1) the association between whole body substrate utilization and the development of obesity and insulin resistance and (2) the relation of metabolic flexibility to tissue specific insulin resistance.
Methods
Male C57Bl/6J mice are susceptible to high-fat diet induced obesity and insulin resistance whereas females are not. Estrogen status was manipulated in order to modulate the development of obesity and insulin resistance. Low estrogen groups consisted of males and ovariectomized females. High estrogen groups consisted of females, ovariectomized females supplemented with estrogen and males supplemented with estrogen. Mice were analyzed after 10 weeks of high fat diet. Metabolic flexibility was determined by indirect calorimetry and was defined as the change in respiratory quotient upon refeeding after fasting. Tissue specific insulin sensitivity was determined by hyperinsulinaemic- euglycaemic clamp analysis using radio labeled isotopes.
Results
Metabolic flexibility was consistently 2-4 fold higher in the high estrogen groups (p<0.05). Metabolic flexibility was positively correlated with insulin stimulated rate uptake of glucose by metabolically active tissues. No correlation was found with insulin mediated repression of glucose production. In addition, metabolically flexible mice had lower fat accumulation.
Conclusion
These data indicate that peripheral insulin sensitivity is reflected by the oxidative substrate selection in response to fasting / mixed meal refeeding and can be modulated by estrogen status.
Obes Facts. 2009 May 14;2(Suppl 2):145.
Background/Aims
A high fat oxidation (low fasting respiratory quotient (RQ)) adds to sustained weight loss in obese subjects. The aim of this study was to analyse changes and possible determinants of fasting RQ after weight loss.
Subjects/Methods
28 non-diabetic overweight and obese females (age: 30.8±6.1 years; BMI: 35.7±4.8kg/m2) were investigated before and after 13.5±2.4 weeks of dietary treatment (1000kcal/d). Body composition was measured by air-displacement plethysmography, visceral fat mass (VAT) by Magnetic Resonance Imaging. Fasting RQ was determined by indirect calorimetry. IS was assessed by a hyperinsulinemic euglycemic clamp (ISM-value) and HOMA2-%S model calculated from basal plasma insulin and glucose levels (ISHOMA2-%S).
Body weight (−9.2±3.9kg; P<0.001), total fat mass (FM) (−8.1±3.6kg; P<0.001) and VAT (−293±278cm3; P<0.001) decreased after weight loss. Basal fasting RQ was 0.84±0.05 (0.73 − 0.93) before and 0.81±0.05 (0.68 − 0.90) after weight reduction. No significant correlations were observed between RQ and FM, VAT or plasma leptin levels before and after weight loss as well as between the changes in these parameters and changes in fasting RQ. Subjects were divided into two group according to changes in insulin sensitivity. Improved IS after weight loss (ISM-value = +1.7±0.9 mg/kg*min; ISHOMA2-%S = +20.9±12.2; n=19) was associated with a significant reduction in fasting RQ (−0.03±0.04; P<0.05) whereas the group with a constant IS (n=9) did not show a change in fasting RQ.
Conclusion
Weight loss was associated with increased basal fat oxidation in women with improved insulin sensitivity only.
Conflict of Interest: None disclosed. Funding: Research relating to this abstract was funded by Deutsche Forschungsgemeinschaft (DFG MU 714/8-3)
Obes Facts. 2009 May 14;2(Suppl 2):145–146.
Introduction
Elevated levels of serum gamma-glutamyltransferase (GGT) are associated with components of the metabolic syndrome and increased risk of cardiovascular and liver diseases in adults. Elevated GGT levels have been found to predict the development of type 2 diabetes in adults, but, in children is unknown. The aim of this study was to investigate whether GGT is independently associated with insulin resistance in obese Korean children.
Methods
A total of 1307 overweight (above the 85th BMI percentile of Korean reference) boys (n=822) and girls (n=485), ages 9-15 years were studied. Measures included weight, height, percent body fat (BF%), waist circumference, blood pressure, fasting glucose and fasting insulin, C-re-active protein, total cholesterol, triglycerides, HDL-Cholesterol, GGT, aspartate aminotransferase (AST), and alanine aminotransferase (ALT). Insulin resistance (IR) was calculated using the homeostasis model assessment (HOMA-IR).
Results
GGT and ALT were positively associated with IR in boys and girls. In multiple regression analysis for HOMA-IR as dependent variable, GGT (β = 0.120; P = 0.048 in boys, β = 0.207; P = 0.003 in girls) and ALT (β = −0.009; P = 0.885 in boys, β = 0.025; P = 0.716 in girls) emerged as determinants of HOMA-IR of the subjects (R2 = 0.102 in boys, R2 = 0.155 in girls) independently of age, BF% and waist circumference.
Conclusions
Serum GGT level is a stronger predictor of IR than ALT in obese children, but whether serum GGT activity predicts the development of type 2 diabetes or cardiovascular disease in obese children remains to be determined.
Obes Facts. 2009 May 14;2(Suppl 2):146.
Introduction
We aimed to explore whether the metabolic syndrome (MS) is associated with abnormal serum levels of PTH, vitamin D and magnesium.
Methods
Fasting serum levels of 25-hydroxyvitamin D [25(OH)D], PTH, calcium, phosphate and magnesium were assessed in 1,017 consecutive morbidly obese patients (68% women) with a mean (SD) age of 42 (12) years and BMI of 44.7 (6.2) kg/m2. MS was diagnosed according to the ATP III criteria. Multiple logistic regression analyses were used to assess the independent effect of PTH, 25(OH)D and magnesium on the odds for MS after adjustments for possible confounders, including calcium, phosphate, creatinine, age, gender, season of serum sampling, BMI, current smoking, albuminuria, CRP, insulin resistance and type 2 diabetes.
Results
Forty-four percent of the patients had MS without diabetes, and 24% had both MS and diabetes. PTH was significantly correlated with systolic blood pressure (r=0.15, P<0.001) and diastolic blood pressure (r=0.14, P<0.001), but not with the other components of MS. Patients with PTH levels in the upper three quartiles had a 1.5- to 2-fold increased odds of MS (First quartile reference, P for trend 0.008). The latter findings were consistent after the exclusion of patients using thiazides, loop diuretics, ACE-inhibitors, A2-antagonists, and vitamin D supplements. The levels of 25(OH)D and magnesium were not associated with MS in the multiple regression analyses.
Conclusions
Elevated serum PTH is independently associated with MS in morbidly obese patients. Randomised controlled clinical trials, including different therapeutic strategies to lower PTH, are necessary to explore any cause-and-effect relationship.
Conflict of Interest: None disclosed. Funding: Hofs⊘ D. has received unrestricted educational grants from Novo Nordisk A/S, Health Region South-East, and the Hospital in Vestfold.
Obes Facts. 2009 May 14;2(Suppl 2):146.
Introduction
Hormone-sensitive lipase (HSL) is one of the two enzymes catalyzing triglyceride hydrolysis in adipocytes. HSL is also the rate-limiting enzyme for diglyceride hydrolysis. In human adipose tissue, HSL protein content correlates with maximal stimulated lipolysis. Expression and activity of HSL is decreased in overweight, obese and insulin-resistant patients.
Methods
We used HSL heterozygous mice (HSL +/-) to examine insulin sensitivity and adipose tissue inflammation under mild lipolytic inhibition. Wild types (WT) and knock out (KO) were used as controls. Mice were administered a high fat diet for 20 weeks.
Results
Lipase and lipolytic activities was 50% lower in adipose tissue of HSL+/- mice than in WT mice. This observation validates the use of the heterozygous mice. Upon high fat diet, HSL+/- and WT mice became obese while HSL KO mice did not. Lipolysis was equally reduced with HFD but HSL+/- mice remained more insulin sensitive than WT mice. Finally, diet induced adipocyte hypertrophy is more pronounced in HSL+/-mice. Analysis of the inflammatory profile of adipose tissue is ongoing.
Conclusion
This animal model highlights that reduced lipolytic capacity can alter insulin sensitivity. Genetic expression of inflammation markers associated with adipocyte secretions will illustrate the impact of lipolysis defect on AT inflammation.
Conflict of interest: None disclosed. Funding: Research relating to this abstract was funded by the European project HEPADIP and INSERM (Poste d'accueil vétérinaire).
Obes Facts. 2009 May 14;2(Suppl 2):146–147.
Introduction
Studies in diabetes-prone rats indicate that obesity-associated insulin resistance can be improved by activation of AMP-activated protein kinase (AMPK). AMPK, a major regulator of cellular energy metabolism, is able to stimulate glucose uptake in muscle - independent of insulin - and to lower triglyceride accumulation in non-adipose tissues. The natural compound alpha lipoic acid (ALA) has been suggested to activate AMPK and to reduce energy intake. Here, we investigate if ALA prevents high-fat induced obesity and improves whole body glucose tolerance. Furthermore, we examine if the improved glucose homeostasis is mediated via improved skeletal muscle insulin signalling.
Methods
Rats were fed low fat (LFD, 10% of energy (E%) from fat) or high fat (HFD, 45 E% fat) diets, supplemented with or without 0.5% w/w ALA for 8 weeks. Body weight and food intake of the animals were monitored weekly. After 8 weeks of dietary intervention, the animals received an intraperitoneal glucose bolus (1.5g/kg) (ipGTT). At week 8.5 rats were sacrificed 9 minutes after an insulin bolus (10u/kg) to obtain insulin-stimulated tissue. Skeletal muscle insulin signalling was studied using western blot analysis of Akt phosphorylation and GLUT4 translocation. AMPK activity and lipid accumulation in skeletal muscle is currently under investigation.
Results:
| LFD | LFD+ALA | HFD | HFD+ALA | |
|---|---|---|---|---|
| Food intake (kJ/week) | 2085±73 | 1496±79 | 2308±65 | 1650±83 |
| Body weight gain (g/week) | 16±2 | 4±3* | 20±3 | 4±2# |
| iAUC glucose (mmol/l*min) | 439±39 | 238±23* | 430±66 | 224±21 |
| iAUC insulin (µg/l*min) | 83±40 | 9±26 | 149±60 | 70±13 |
| Ser473Akt/total Akt (arbitrary OD units) | 1.1±0.2 | 1.1±0.2 | 1.2±0.3 | 1.3±0.3 |
| GLUT4 membrane fraction (arbitrary OD units) | 2.0±0.7 | 2.0±0.6 | 1.4±0.6 | 1.3±0.8 |
Data are mean±SE, n=8, * p < 0.05 vs. LFD, # p < 0.05 vs. HFD
Conclusion
ALA supplementation had a pronounced decrease on food intake and body weight. In addition, whole body glucose tolerance was higher after 8 weeks of ALA treatment independent of the fat content of the diet. Although whole body glucose tolerance was improved, no effect was seen on skeletal muscle insulin signalling.
Obes Facts. 2009 May 14;2(Suppl 2):147.
Introduction
Accumulation of lipid intermediates in skeletal muscle is associated with the development of muscular insulin resistance. Interestingly, fasting also leads to insulin resistance. Whether the mechanisms underlying are comparable, is unknown.
Methods
7 healthy subjects (age 25±4.4 yrs (mean±SD), BMI 22.2±1.94 kg/m2, VO2max 3.76±0.22 L/min) underwent in random order a 60h fast (calorie-free drinks only (S)) or a control diet (50-35-15% of energy as CHO, fat and protein (FED)). During the study, subjects stayed in a respiration chamber to measure energy expenditure and substrate oxidation. Insulin-sensitivity was assessed using a hyperinsulinemic-euglycemic clamp. Muscle biopsies and blood samples were taken after each intervention period in basal and insulin-stimulated conditions but have not been analyzed yet.
Results
Sleeping RQ, measured during the three nights in the respiration chamber, did not change in the FED condition (0.84±0.02, 0.82±0.05 and 0.83±0.03). In the S condition, the RQ dropped (0.84±0.03, 0.77±0.01 and 0.75±0.01). Metabolic flexibility - defined as the increase in RQ upon insulin stimulation - was reduced (delta RQ: 0.13±0.05 vs. 0.05±0.03 in FED and S, p<0.05). Insulin sensitivity (m-value) was significantly reduced after fasting by 48.2%±13.8.
Conclusion
In young healthy subjects 60 hours of fasting increases fat oxidation, induces severe insulin resistance and metabolic inflexibility. Whether these findings are explained by similar mechanisms as seen in obesity related insulin resistance is currently under investigation.
Conflict of Interest: None Disclosed. Funding: Research relating to this abstract was funded by TI Food & Nutrition
Obes Facts. 2009 May 14;2(Suppl 2):147.
Introduction
To prescribe individualized exercise intensities, the individual maximal aerobic capacity (peak oxygen uptake: VO2peak) may be measured. To assess VO2peak, a graded exercise test (GXT) to volitional exhaustion must be performed. However, maximal GXT must be avoided as far as possible in certain obese patients (e.g., hypertensive obese patients), because the high exercise intensities increase the cardio-vascular event risks. Consequently, a method determining VO2peak during sub-maximal GXT must be proposed. The purpose of this study was to test the validity of predicting VO2peak from Ratings of Perceived Exertion of Borg (RPE), during a sub-maximal GXT, in obese women.
Methods
Forty-three obese women performed GXT to volitional exhaustion. GXT was carried out on a cycle ergometer, with an initial resistance set at 10W and increments of 10W.min−1. At the volitional exhaustion, the actual VO2peak was determined. During GXT, oxygen uptake (VO2) and RPE were measured to draw the individual linear regressions between VO2 and RPE≤15. These regressions were extrapolated to RPE=20 (i.e., the maximal value on the RPE scale) to predict VO2peak.
Results
Actual and predicted VO2peak were not significantly different (13.9±3.0 vs 14.2±3.3ml.kg−1.min−1, respectively; p=0.26). The Pearson product moment correlation between actual and predicted VO2peak was high (r=0.82). The 95% limits of agreement analysis on these values (bias±2SD) was −0.3±3.7ml.kg−1.min−1.
Conclusion
Results suggested that RPE≤15 elicited during a sub-maximal GXT provided accurate VO2peak prediction. Therefore, it is not necessary to perform maximal GXT to determine the maximal aerobic capacity in obese women.
Conflict of Interest: None Disclosed. Funding: Research relating to this abstract was funded by the “Programme Régional de Santé” and the “Programme National de Nutrition et de Santé”.
Obes Facts. 2009 May 14;2(Suppl 2):147–148.
Introduction
Mitochondria are the central machinery which regulate energy metabolism. The aim of this study is the characterization of mitochondrial function and proteome of adipose tissue in obese animals and subjects.
Methods
White adipose tissue from diet-induced obese mice and visceral adipose tissue from obese non-diabetic, obese diabetic and control patients was analysed to characterise the mitochondrial function through the use of High Resolution Respirometry (Oroboros®). Samples were permeabilised and mitochondrial oxygen consumption was measured using different drugs to study the activity of the OXPHOS complexes. Highly pure mitochondria were purified from animal adipose tissue and analysed by proteomics using DIGE technology. Western blot was assessed with human adipose tissue proteins to study the mitochondrial content of the samples.
Results
Mitochondrial oxygen consumption was decreased in white adipose tissue obese mice and humans. DIGE analysis of highly pure mitochondrial protein from mouse samples showed differential expression profile between phenotypes. Western blot analysis demonstrated no changes in mitochondrial content of obese non-diabetic patients, but a decrease in obese diabetic patients.
Conclusion
These results demonstrate a reduction in mitochondrial oxygen consumption in adipose tissue of both obese animals and humans. In obese non-diabetic humans, posttranslational modifications and/or changes in other non-proteic components of the OXHOS system, may account for this modified activity. On the contrary, in obese diabetic patients, the most prevalent mechanism would be a reduction in the adipose mitochondrial content. In both situations, the consequence would be a net reduction in adipose tissue mitochondrial oxygen consumption.
Funding: Research relating to this abstract was funded by the Instituto de Salud Carlos III (CP07/00152).
Acknowledgments
We thank Dr. Josep Vidal and Dr. Francesc Carmona for their helpful assistance in human sample compilation.
Obes Facts. 2009 May 14;2(Suppl 2):148.
Introduction
Since weight loss reduces energy expenditure, we hypothesized that it might be affected by macronutrient composition of the diet. POUNDS LOST was a prospective, randomized controlled trial in 811 people comparing four diets differing in fat, protein, and carbohydrate content. Participants were 811 overweight men (M) and women (F).
Methods
Total daily energy expenditure (TDEE) was measured in a subset of 99 participants at baseline and 89 at 6 months. Participants from each diet group received doubly-labeled water and resting energy expenditure (REE) was measured by hooded canopy (N=99).
Results
Body weight declined by 8.13 kg with M losing significantly more than F (p=0.0062), but with no differences between the four diets. Weight loss reduced TDEE by 110 kcal/d in M and 130 kcal/d in F and REE by 138 kcal/d in M and 129 kcal/d in F. Energy expenditure from activity (PAEE) did not change significantly from baseline (+ 50 kcal/d in M; 16 kcal/d in F) and there was no differential effect of the four diets on PAEE, REE, or TDEE. REE remained strongly related to body weight and fat-free mass. TDEE and REE were related to total body weight and fat-free mass (FFM), but not body fat. Macronutrient composition of the diet did not affect the magnitude of the changes in energy expenditure.
Conclusion
We conclude that the decline in energy expenditure with weight loss is due to a decrease in REE with no change in activity and that diet composition during weight loss does not have a differential effect.
Conflict of Interest: none disclosed. Funding: United States Public Health Service grant U01HL 73286 from the National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD
Obes Facts. 2009 May 14;2(Suppl 2):148.
Introduction
High-fat (HF) diet is known to be a strong obesogenic stimulus. Its effect can be counterbalanced by stimulation of energy expenditure and lipid oxidation in response to the meal. Aim of this study was to reveal whether muscle nonshivering thermogenesis could be stimulated by HF diet. The other aim was to support the hypothesis of leptin and AMP-activated protein kinase (AMPK) involvement in this mechanism.
Methods
Male mice of obesity-resistant A/J and obesity-prone C57BL/6J (B/6J) strains, born and maintained at 30 oC, were used. At 4 weeks of age, mice were randomly weaned onto a low-fat (LF) or HF diet. At the age of 6 weeks, indirect calorimetry and cold tolerance test were performed and tissues for in-vitro experiments, biochemical and gene expression analysis were collected.
Results
The A/J LF mice were cold-sensitive, while the A/J HF, B/6J LF and B/6J HF mice were cold-tolerant. Cold-sensitivity of the A/J LF mice was associated with low energy expenditure, which was normalized by HF diet. Only in A/J mice, oxygen consumption, total content and phosphorylation of AMPK, and AICAR-stimulated palmitate oxidation in soleus muscle was increased by the HF diet in parallel with significantly increased leptinemia. Gene expression data in soleus muscle of the A/J HF mice indicate a shift from carbohydrate to lipid oxidation.
Consclusion
Our results suggest a role of muscle nonshivering thermogenesis and lipid oxidation in the obesity-resistant phenotype of A/J mice and indicate that HF diet could induce thermogenesis in oxidative muscle, possibly by the leptin-AMPK axis.
Obes Facts. 2009 May 14;2(Suppl 2):148–149.
Introduction
Skeletal muscle exhibits metabolic flexibility. Under fed condition it uses glucose whereas during fasting it oxidizes lipids. In type 2 diabetic patients, the failure of a such switching is associated to intramuscular triglyceride accumulation (lipotoxicity) and insulin resistance. Some members of the MAPK family are implicated in the downregulation of insulin action and signaling. We have shown that Erk1-/- mice are resistant to high fat diet-induced obesity and protected from insulin resistance. Moreover, they display a higher post-prandial metabolic rate and are protected against lipotoxicity. Here, we investigate Erk1-/- skeletal muscle oxydative capacity to determine whether Erk1 invalidation could protect from lipotoxicity.
Methods
Ten weeks old Erk1-/- mice are sacrified after 16h of fasting. Protein expression is determined by Western Blotting and enzymatic activity with commercial kits.
Results
Under fasting, a situation rising fatty acid flux, Erk1-/- muscles display a higher expression of proteins involved in fatty acid oxidation (M-CPT1, MCAD) and in oxydative phosphorylation (complexes 1, 2, 4; cytochrome C; UCP3). Furthermore, mitochondrial complex activity and expression of transcription factors regulating fatty acid oxidation steps (PGC1, PPARa, ERRa, MEF2) are higher in Erk1-/- muscles. AMPK is an important energy sensor which activation promotes fatty acid oxidation by phosphorylating Acetyl CoA Carboxylase (ACC). Phospho AMPK and phospho ACC expression is increased in Erk1-/- muscles.
Conclusion
Erk1 invalidation seems to induce an increased oxidative capacity that could protect from lipotoxicity and improve insulin sensitivity. Thus, targeting specifically Erk1 may represent a new pharmacological strategy to fight obesity and insulin resistance.
Obes Facts. 2009 May 14;2(Suppl 2):149.
Introduction
Endurance training at an intensity eliciting maximal fat oxidation may have a beneficial effect on body weight and glucose metabolism in obese patients. However, the exercise intensity at which maximal fat oxidation occurs and the factors limiting fat oxidation are not well studied in this population.
Methods
We studied 98 overweight / obese, healthy, drug-free volunteers (age: 43.6±8.9, BMI: 33.8±3.6). Abdominal fat distribution, intramuscular (IMCL) and intrahepatic lipid content were assessed by magnetic resonance imaging. An incremental exercise test with indirect calorimetry was performed to estimate exercise capacity and substrate oxidation. Furthermore, resting blood pressure and body composition (bio-impedance analysis) were measured and venous blood samples were collected.
Results
Maximal exercise-induced fat oxidation was 0.31±0.03 g × min−1 in men and 0.23±0.02 g × min−1 in women (p<0.05). Exercise intensity at the maximum fat oxidation was 41.5 ± 2.5%VO2max in men and 43.7 ± 1.9%VO2max in women. With multivariate analysis, maximal fat oxidation was related to fat free mass, percent fat mass, and oxidative capacity, but not to absolute and visceral fat mass, or IMCL.
Conclusion
Obese subjects seem to have a limited capacity to oxidize fat during exercise, and achieve maximal fat oxidation at already lower exercise intensities. The capacity to oxidize fat during exercise in obesity appears to be limited by skeletal muscle mass and oxidative capacity rather than the availability of visceral fat or IMCL.
Conflict of Interest: None disclosed. Funding: This work was supported by grants from the Federal Ministry of Education and Research (BMBF-0313868) and the Commission of the European Communities (Collaborative Project ADAPT, Contract No. HEALTH-F2-2008-201100).
Obes Facts. 2009 May 14;2(Suppl 2):149.
Introduction
Sustained increases in energy intake above energy expenditure (overfeeding) not only result in increases in lean and fat mass but also are hypothesized to increase energy expenditure. Initially termed luxusconsumption by Neumann, there has been great controversy on the magnitude of this effect and its contribution to homeostatic control of body weight regulation. The purpose of this study was to explore the effect of medium-term overfeeding on resting energy metabolism.
Methods
Six healthy young men and three women aged 18 − 28 with a BMI of 25.7 + 0.99 were admitted to the inpatient unit and consumed a weight maintaining diet. Energy requirements were determined by whole room calorimetry and weight stability over 2 weeks. At baseline, overnight fasted REE and RQ were measured by indirect calorimetry. Subjects then consumed a diet consisting of 44 %fat, 15% protein and 41% carbohydrate for 4 weeks at +40% of energy requirements and RMR/RQ were measured weekly thereafter.
Results
REE, as a percent change from baseline, increased during overfeeding: W1 1.59 + 2.04%; W2 4.83 + 3.33%; W3 3.62 + 1.82%; W4 7.93 + 2.92 (p< 0.05). RQ did not significantly change over the study period.
Conclusion
These results suggest that the increase in energy expenditure with overfeeding is small and early and increases as the duration of overfeeding increases. This result supports the observations of Neumann that there is a small, but measurable increase in resting energy expenditure which occurs with overfeeding but that transient short-term overfeeding will produce only trivial luxusconsumption.
Conflict of Interest: None Disclosed. Funding: Research relating to this abstract was funded by the United States Department of Agriculture.
Obes Facts. 2009 May 14;2(Suppl 2):149.
In order to establish a relationship between leptin resistance and ectopic deposition of lipids, we have characterized the evolution of i) white adipose tissues (WAT), heart and liver weights, ii) triglyceride (TG) content in heart and liver, and iii) responsiveness to acute leptin in these tissues/organs. The study was carried out in C57BL6J mice treated with a high-fat (HF) diet during 8, 14 and 32 weeks (DIO). Leptin resistance was estimated by measuring phosphorylation of STAT3 in tissues/organs from animals receiving 1 mg/kg leptin.
Results
Relative weight of lumbar WAT increased 40%, 46% and 21% after 8, 14 and 32 weeks on treatment. A similar evolution was detected in mesenteric WAT. The liver exhibited an initial 32% decrease after 8-week treatment, followed by a 20% and 32% increase after 14 and 32 weeks, respectively, which was coincident with an increase of TG content in this organ. No significant effect was detected in the heart. HF induced hyperleptinemia regardless the duration of the dietary treatment and hyperinsulinemia was observed from 14-week HF. Leptin resistance developed progressively in liver and WAT after 14-week HF but the heart kept leptin responsiveness at this time-point.
Conclusion
This study provides a longitudinal characterization of the evolution of metabolic parameters during the development of DIO. Our data show that the onset of leptin signalling disruption within the liver is coincident with the onset of hepatic steatosis and suggest that the liver acts as a secondary trap which becomes operative when TG accumulation in WAT is impaired.
Disclosure Statement
The authors have nothing to disclose
Funding: MCI (SAF 2006-02456 and SAF 2005-0518), FUSP-CEU and SESCAMET.
Obes Facts. 2009 May 14;2(Suppl 2):149–150.
Introduction
We previously showed that overexpression of neuropeptide Y (NPY) in the sympathetic nervous system and brain noradrenergic neurons increases adipose tissue mass and hepatic triglyceride accumulation in transgenic (NPY-OEDBH) mice (Ruohonen et al, Diabetes 57:1517, 2008). This study tested the hypothesis that increased copy number will enhance the metabolic phenotype of NPY-OEDBH mice.
Methods
Transgene homozygous and wildtype (WT) control mice (n = 7-11/group) were generated by breeding transgene homozygous and negative siblings genotyped by real time PCR. Weight gain was monitored weekly. Intraperitoneal glucose (1 g/kg) and insulin (0.5 IU/kg in females, 1.0 IU/kg in males) tolerance tests were performed and food consumption and 24 h locomotor activity measured at 3 months of age. Adipose tissue mass, plasma insulin and total cholesterol were measured after sacrifice.
Results
White adipose tissue weight was increased by 61% in male (P < 0.001) and by 43% in female (P < 0.05) NPY-OEDBH mice compared to WT mice. However, body weight gain, food intake or physical activity were not significantly changed in the NPY-OEDBH mice. Glucose tolerance was impaired in both female and male NPY-OEDBH mice. Male transgenic mice showed also insulin resistance and increased fasting blood glucose. Serum insulin was not and cholesterol tended to be increased in NPY-OEDBH mice compared to WT controls.
Conclusions
Homozygous overexpression of NPY in noradrenergic neurons leads to more pronounced metabolic phenotype than hemizygous overexpression with increased adiposity and impaired glucose tolerance, and provides a novel mouse model of metabolic syndrome associated traits
Conflicts of interest: none. Funding: Turku University Foundation
Obes Facts. 2009 May 14;2(Suppl 2):150.
Background
Ghrelin inhibits sympathetic nervous system (SNS) activity in rodents, but its effect on healthy humans, in obesity or in vagotomized subjects are unknown.
Subjects
7 lean (mean body mass index (BMI) 23.6 +/-0.9 kg/m2), 7 morbidly obese (mean BMI 50.9 +/-4.4 kg/m2) and 7 post-gastrectomy subjects (mean BMI 22.0-±1.1 kg/m2).
Interventions
Subjects were randomized to intravenous ghrelin (5 pmol/kg/min) or saline over 270 minutes. Subjects had a fixed calorie meal and a free choice buffet at the end of the infusion. Heart rate variability (HRV) was measured at regular intervals.
Results
Using ANOVA, ghrelin had an overall highly significant inhibitory effect on total power (TP) (p=0.001), high frequency (HF) power (p=0.04), very low frequency (VLO) power (p=0.03) and no effect on low frequency (LF) (p=0.07). Ghrelin had a significant effect on TP (p=0.03), borderline effect on LF power (p=0.06) and no effect on HF power (p=0.1) in healthy controls. By contrast in obese subjects, ghrelin had no effect on TP (p=0.3), LF (p=0.5) and HF (p=0.06) and also no effect in the vagotomized subjects on TP (p=0.7), LF (p=0.7) and HF (p=0.9). Ghrelin had no effect on the LF/HF ratio.
Conclusions
Ghrelin inhibits SNS activity in healthy controls with a moderate effect on PNS activity but had no effect on obese subjects. Vagotomized subjects also did not respond to ghrelin suggesting the vagus nerve is important for the effects of peripheral ghrelin on the SNS.
Conflict of interest: None. Funding: This project was funded by Pharmacia.
Obes Facts. 2009 May 14;2(Suppl 2):150.
Objective
The study objective was to identify relationship between circadian rhythm of blood pressure and glucose tolerance status in non-diabetic, clinically severe obese patients
Methods
40 consecutive, non diabetic patients with morbid obesity (BMI < 45 kg/m2) aged 25-57 before bariatric surgery underwent metabolic profiling, a 75 g oral glucose tolerance test (OGTT) and 24-h ambulatory blood pressure monitoring (24-h ABPM).
Results.
15 patients had impaired glucose tolerance (IGT) and 25 normal glucose tolerance (NGT). All patients had hypertension. The prevalence of non-dipping blood pressure pattern was 26,67% in the IGT group and 48% of the NGT group. The mean diurnal-nocturnal differences of average systolic blood pressure were 19,2 and 15,28 mmHg. Statistic analysis did not show significant effect of IGT/NGT on blood pressure pattern, but revealed % fat mass to have significant effect for predicting it
Conclusion:
% fat mass have significant effect for predicting non-dipping blood pressure pattern
here is no relation between glucose tolerance status and blood pressure pattern in non–diabetic, clinically severe obese patients
Adequate antihypertensive therapy in severe obese patients should aim also at re-establishing the physiological nocturnal BP fall.
Obes Facts. 2009 May 14;2(Suppl 2):150.
Introduction
Reducing the glycaemic index (GI) of the diet may decrease metabolic risk, primarily through reduction and stabilisation of blood glucose. The aim of this study was to investigate whether incorporation of lower or higher GI foods into mixed meals had different effects on day-long glucose profiles, measured in interstitial fluid by a continuous glucose monitoring system (CGMS).
Methods
The study was a randomised balanced 2-way crossover intervention of 2 × 1-week periods of lower and higher GI diets. Subjects were 12 overweight healthy adult women (BMI 27.5 (SD 2.3) kg/m2). Changes in GI were achieved through substitution of key staple carbohydrate-rich foods. After 4 days run-in on each dietary regimen, subjects wore the CGMS over 2 identical controlled feeding days in the laboratory, separated by 1 day of ad libitum consumption at home.
Results
On controlled days, diets differed in GI by 15 units and provided equal energy, macronutrients and fibre. On ad libitum days, diet diaries revealed a difference in GI of 14 (SE 1) units, with no significant difference in energy, macronutrient or fibre intake. No differences were observed in glucose profiles between higher and lower GI interventions, either in the controlled or the ad libitum setting. There was significant agreement in area under the glucose curve on repeated controlled feeding days (intra-class correlation = 0.75).
Conclusion
This study indicates that a difference in dietary GI of 14-15 units is insufficient to alter day-long glycaemia, as measured in interstitial fluid, in the absence of broader dietary changes.
Conflict of Interest: None Disclosed. Funding: Research relating to this abstract was funded by the Medical Research Council
Obes Facts. 2009 May 14;2(Suppl 2):151.
Obesity is associated with lower B-type natriuretic peptide (BNP) levels in healthy individuals. Its relationship with fat mass and LV hypertrophy is not well documented.
Objective
The study objective was to identify relationship between NT-proBNP and body mass index, fat mass, LV hypertrophy in clinically severe obese patients without diabetes
Methods
30 consecutive, non diabetic patients with morbid obesity (BMI < 45 kg/m2) aged 25-57 before bariatric surgery underwent measurement of body mass, body composition by direct dual energy x-ray absorptiometry (DEXA), NT-proBNP, echocardiography. Patients with diagnosis of congestive heart failure (CHF), chronic kidney disease (CKD) and diabetes were excluded. All patients had hypertension, but none of them was exposed to beta-blokers.
Results
Of obese patients without CHF, CKD, diabetes, 16,66% (5 of 30) had NT-proBNP concentrations greater than 125 pg/ml. Statistic analysis show that BMI was independently associated with lower NT-proBNP (p<0.001). Fat mass and % fat mass were not correlated with its values. LVMI correlated positively with NT-pro BNP (p< 0.005)
Conclusion
In morbidly obese patients without diabetes we confirm the previously described association between higher BMI and lower NT-proBNP and unknown lack of association between NT-pro BNP values and both fat mass and % fat mass. In studied group, NT –proBNP appears useful for evaluating LV hypertrophy.
Obes Facts. 2009 May 14;2(Suppl 2):151.
Introduction
The predominance of small dense LDL (LDL phenotype B) has been accepted as an emerging cardiovascular risk factor by the adult treatment panel III (Berneis 2004) and is a component of the lipid triad associated with metabolic syndrome (MetS) and diabetes (Austin 1991).
Methods
Subject with MetS were recruited. The analysis was done on the subgroup of the LIPGENE Human Dietary Intervention Study (n=99). Antropometric characteristics, glucose tolerance parameters, plasma lipid, lipoprotein and apolipoprotein profile was reported. The association between the genotyped polymorphisms and basal pre-dietary LDL density and switch from low to high, atherogenic LDL density (phenotype B) were studied by Cochrane-Armitage trend test.
Results
LDL phenotype B is determined by triglyceride level (TG), not by cholesterol (TC). Plasma level of Triglyceride Rich Lipoprotein (TRL TG, TRL C), ApoB100, ApoB48, ApoCIII and glucose is higher in contrast to low plasma ApoAI in LDL phenotype B carriers compared to phenotype A in studied cohort. The list of SNPs with their gene allocation significantly associated with phenotype B concerns: apoprotein AI, CIII, E, H; ATP-binding cassette member 1, fatty acid binding protein 3, PPARGC1A, adiponectin receptor, CD36, cubilin, perilipin, estrogen receptor, insulin-like growth factor 1 receptor, insulin degrading enzyme, glycogen synthase and IL6.
Conclusion
The most prominent role in affecting LDL density phenotype can be assigned to genes that are controlling carbohydrate metabolism as well as genes controlling together lipid and carbohydrate metabolism
Funding: Research relating to this abstract was funded by EU FP6 FOOD-CT-2003-505944 LIPGENE project.
Obes Facts. 2009 May 14;2(Suppl 2):151.
Introduction
Both humans and laboratory rodents are susceptible to the development of obesity when fed a high fat diet but the reason for this diet sensitivity is unclear. We investigated the effects of diet on 5HT and dopamine (DA) release and the response to enterostatin, a peptide known to inhibit fat intake.
Methods
Rats were fed either a high fat (HF; 45% energy fat) or low fat (LF; 11% energy fat) diet for 3-10 days. Striatal slices were preloaded with [3H]-5HT or [3H]-DA and then superfused in a Brandel 1100 Suprafusion system in the presence or absence of enterostatin and either the 5HT reuptake blocker fenfluramine or the DA reuptake blocker nomifensine and the release of [3H]-5HT and [3H]DA assayed at 2 minute intervals for 50 minutes.
Results
The release of DA from striatal slices of animals fed HF diet for 8-10 days was lower than from LF fed rats. Enterostatin increased DA release only from the striatum of HF fed rats and not from LF fed rats. Neither diet nor enterostatin had major effects on 5HT release. No HF diet effect on 5HT release was present when slices were prepared from rats that had received the HF diet for only 3 days.
Conclusion
The reduction in DA release in response to a high fat diet may be implicated in the propensity to overconsume such diets and develop obesity. The mechanism(s) of this diet effect on DA release and enterostatin response is (are) not known at this time.
Conflict of interest: None. Funding: research relating to this abstract was funded by the Utah Science, Technology and Research (USTAR) program.
Obes Facts. 2009 May 14;2(Suppl 2):151–152.
Introduction
Accelerated growth in infancy after slow growth during foetal and early life (catch-up growth) are linked to the development of obesity, insulin resistance and coronary heart disease.
Methods
Offspring born from female C567Bl/6 mice were divided at 3 weeks of age into low (LBW) and high birth weight (HBW) male and female mice groups and weaned onto a standard chow diet (fat content 3%) for 12 weeks. Whole body and liver 1H MRS were performed at 11 and 14 weeks of age at 4.7T using a VMRIS scanner.
Results
LBW males and females showed reduced body weight compared to HBW males and females, during the first 3 weeks of life. LBW males and LBW females started to catch-up weight by week 7. Differences in lengths were significant at week 1 in both LBW vs. HBW males and females. LBW males caught up length by week 7 and LBW females by week 3. At 11 and 14 weeks of age, total percentage adiposity was not significantly different between groups. However, there was a discrete increment in adiposity and IHCL in the LBW males at week 11. Moreover, LBW female mice had significantly higher IHCL compared to HBW females at week 11.
Conclusion
Catch-up growth influences body lipid content in mice born small for their gestational age, being more susceptible to fat deposition in a time-dependant rate. Adaptations in body composition at early age, could lead to long-term detrimental fat distribution.
Conflict of Interest: None Disclosed. Funding: Medical Research Council UK, Chelsea & Westminster Hospital NHS Foundation Trust
Obes Facts. 2009 May 14;2(Suppl 2):152.
Introduction
Growth hormone(GH) is an important regulator of growth and body composition. It has been shown that GH-release can be promoted by administration of various amino acids, such as arginine and lysine, that are present in soyprotein. We previously showed that GH release can be promoted by oral ingestion of soyprotein, it is not known however to which extent other proteins stimulate the GH secretion.
Methods
Ingestion of soy protein(SOY), gelatin protein(GELATIN), alpha-lactalbumin protein(ALPHA-LAC) and milk protein(MILK) were compared on their GH-secretory capacity. After oral ingestion of the protein(0.6 gram protein per kg bodyweight), blood was sampled every 20 min for 5h to analyse GH-, amino acid-, insulin- and glucose-concentrations. The study was performed in eight healthy women(age:19-26y, BMI:19-26 kg/m2) in a randomized, single blind, placebo-controlled crossover design.
Results
GH-responses, area under the curve(AUC) as well as peak-values, were increased after ingestion of GELATIN(8.2±1.1µg/L) compared with ingestion of SOY, ALPHA-LAC, MILK and placebo(5.0±0.8µg/L, 4.5±0.6µg/L, 6.4±1.0µg/L, 2.2±0.8µg/L respectively)(p<0.05). After ingestion of each protein, GH responses were higher compared with placebo ingestion(p<0.05). Simultaneously ingestion of GELATIN resulted in the highest serum-arginine-concentrations(ARG) compared with ARG after ingestion of the other proteins(p<0.05). Insulin as well as glucose responses after ingestion of the proteins were not different between the different proteins(p<0.05).
Conclusion
The GH-promoting activity of protein depends on the protein-source, in that, gelatin protein is the most potent GH stimulator and serum arginine concentrations could be responsible for this effect.
Conflicts of interest: None disclosed. Funding: Research relating to this abstract was funded by TIFood & Nutrition, Wageningen, The Netherlands.
Obes Facts. 2009 May 14;2(Suppl 2):152.
Introduction
Growth hormone(GH) is an important regulator of growth and body-composition. It has been shown that GH-release can be promoted by administration of various amino acids, such as arginine and lysine, that are present in soyprotein. Soyprotein ingestion increases GH-secretion to a higher extent than ingestion of a combination of arginine and lysine. The GH promoting effect of soyprotein however is not present when soyprotein is ingested combined with carbohydrate and fat. The question is whether carbohydrate or fat eliminates the GH-promoting effect of soyprotein.
Methods
We compared ingestion of soyprotein plus carbohydrate(so y+carbohydrate) or soyprotein plus fat(soy+fat) with ingestion of soy alone(soy) and soy plus carbohydrate plus fat(soy+carbohydrate+fat). The study was performed in eight healthy women(age:19-26y, BMI:19-26 kg/m2) in a randomized, single blind, placebo-controlled crossover design.
Results
Ingestion of soy combined with either carbohydrate or fat stimulated GH-responses to the same extent than soy(374±50µg/L.5h, 400±57µg/L.5h, 403±73µg/L.5h respectively), but more than after ingestion of soy+carbohydrate+fat or placebo(water)(226±43µg/L.5h, 84±52µg/L.5h respectively)(p<0.05). Insulin responses were higher after ingestion of soy+carbohydrate or soy+carbohydrate+fat(4745±438U/L.5h, 5462±630U/L.5h respectively), than after soy+fat or soy (2029±478U/L.5h, 2600±255U/L.5h respectively)(p<0.05). Compared with placebo(−256±166U/L.5h), all conditions showed higher insulin responses(p<0.05). Glucose-responses were higher after ingestion of soy+carbohydrate(285±70mmol/L.5h) than after soy+carbohydrate+fat, soy+fat, soy or placebo(75±44mmol/L.5h, −50±38mmol/L.5h, 96±51mmol/L.5h, 9±47mmol/L.5h respectively)(p<0.05). Despite the differences in insulin- and glucose responses between soy+carbohydrate and soy+fat, GH-responses did not differ between soy+carbohydrate and soy+fat.
Conclusion
The GH-promoting activity of soyprotein depends on the macronutrient composition, in that, fat and carbohydrate should not be present at the same time.
Conflicts of interest: None disclosed. Funding: Research relating to this abstract was funded by TIFood & Nutrition, Wageningen, The Netherlands
Obes Facts. 2009 May 14;2(Suppl 2):152.
Introduction
Individuals with a certain personality might be at risk to develop the metabolic syndrome. In our experiments we focus on the differences between so-called proactive and passive personalities.
Methods
Rats selected for either a passive or a pro-active personality were subjected to a series of intravenous glucose tolerance tests (IVGTT) under different dietary (chow or a palatable medium fat diet) and environmental (ability to perform exercise in a running wheel) conditions.
Results
Rats with a passive personality are more sensitive for overeating and weight gain on a palatable medium fat diet. They are also prone to become insulin resistant, reflected by elevated baseline insulin levels and an increased insulin response to an IVGTT under medium fat conditions. Rats with a pro-active personality are normo-insulinemic and relatively resistant to overeating and weight gain. On the palatable diet only passive rats increase their activity levels when they are allowed to exercise. This increase in exercise normalized elevated insulin levels. Pro-active rats do not increase their activity when they are allowed to exercise on a palatable medium fat diet.
Conclusion
We conclude that individuals with a passive personality are more susceptible for insulin resistance and weight gain on a palatable fat diet. But when allowed to exercise these individuals increase their activity leading to markedly improved health. Pro-active personalities are more resistant to weight gain and insulin resistance on a fat diet, but if they are already overweight they will not compensate weight gain with increased physical activity.
Obes Facts. 2009 May 14;2(Suppl 2):153.
Introduction
In vitro studies using rat or human visceral adipocytes reveal opposite effects of TSH on leptin secretion, showing either suppression or stimulation, respectively. There are no in vivo evidence about the TSH effects on leptin secretion in humans. The aim of this study was to measure the changes of serum leptin after administration of recombinant human TSH (rhTSH) in patients with differentiated thyroid cancer.
Methods
One hundred patients [77 females and 23 males; mean age 47 + 13 range 16-76 years, mean body mass index (BMI) 26.8 + 6.3 range 17.4-62.4 Kg/mq] already treated with total thyroidectomy and 131I remnant ablation were enrolled. Each patient received a standard dose of 0,9 mg rhTSH i.m. for two consecutive days according to the conventional protocol. Blood samples were taken for the dosage of TSH and leptin before the first administration of rhTSH as well as 24, 48 e 72 h after the second administration.
Results
Mean serum leptin increased by total 13.9%, 19.1%, 12.2% at 24, 48 and 72 h, respectively. The effect of rhTSH stimulus was studied by a time-average analysis [area under the curve (AUC)]. Significant positive correlations of leptin-AUC with respect to basal leptin (R 0.411; p<0.0005) and BMI (R 0.368; p<0.0005) were observed.
Conclusion
rhTSH administration induces leptin secretion especially in subject with elevated BMI and high levels of adiposity. The role that TSH plays in physiological conditions to regulate leptin secretion remains a matter of investigation.
Obes Facts. 2009 May 14;2(Suppl 2):153.
Aims
To evaluate differences in resistin levels between women with and without metabolic syndrome (MetS) and to assess correlations of resistin with indexes of insulin resistance (IR) and with parameters considered for the MetS definition.
Methods
We studied 132 premenopausal women (83 obese). They were anthropometrically characterized, blood pressure (BP) assessed and a blood sample was collected in the fasting state for glucose, HDL-c, triglycerides, insulin and resistin determinations. We considered the IDF definition of MetS and three indexes of IR: HOMA-IR, QUICKI and McAuley index (McAULEY).
Results
Patients were characterized by mean age=34.9±7.8 years, BMI=35±12.4 Kg/m2, waist circumference=100.2±25.8 cm, percentual fat mass (%FM)=39±12%, systolic BP=117.4±18.4 mmHg, diastolic BP=75.5±12.2 mmHg, glucose=93±27.5 mg/dl, HDL-c=58.1±16.3 mg/dl, triglycerides=107.5±72.3 mg/dl, insulin=11.3±6.6 µU/l, resistin=21.4±9.8 ng/ml, HOMA-IR=2.73±2.1, QUICKI=0.15±0.02 and McAULEY=7.59±2.23. There were significant differences, between obese and non-obese women, for the parameters assessed (p=0.044 for resistin; p<0.001 for all the others). Comparing those with and without MetS, we didn't found significant differences in resistin levels but there were for all other parameters (p<0.001). Resistin was directly and significantly correlated with BMI (p=0.001; r=0.288), waist (p=0.002; r=0.268) and %FM (p=0.002; r=0.272); a negative association was present with QUICKI (p=0.019; r= −0.204) and McAULEY (p=0.015; r= −0.211) which disappear after correction for anthropometry. Similar results were observed when we considered only the obese women.
Conclusion
Higher resistin levels are associated with an excess of fat mass. However, in premenopausal women, resistin is not a good marker of IR and it is a bad indicator for the presence of the MetS.
Obes Facts. 2009 May 14;2(Suppl 2):153.
Introduction
Metformin is an insulin sensitizer with vascular protective effects. Despite multiple pathways of action being proposed, the mechanism of action of metformin is not fully understood. We investigate if adiponectin and its receptors are involved in metformin actions.
Methods
In vivo study 22 insulin resistant obese subjects were randomized to a 3-months treatment with metformin (850 mg BID) + lifestyle intervention (ML) or placebo+ lifestyle intervention (PL). Before and after treatment OGTT, a blood collection for lipids, insulin and adiponectin were performed and periumbilical subcutaneous adipose tissue (SAT) specimens were obtained to investigate expression of adiponectin, AdipoR1 and AdipoR2 (real-time PCR). In vitro study Five SAT explants were used to assess the in vitro effects of metformin (10 mmol for 1 and 24 hr).
Results
Compared to baseline, BMI and waist circumference decreased by 9.9% and 3.4% in ML group and by 5.7% and 2.1% in PL group (p<0.05). After adjustment for BMI changes, metformin significantly increased the effect of lifestyle intervention on SAT expression of AdipoR1 and AdipoR2 (p<0.05 for both) and tended to increase that of adiponectin (NS). Both ML and PL did not modify serum adiponectin levels. In SAT explants, Adipo R1 and R2 expression increased by 53% and 15% respectively after 24h of metformin stimulation. Adiponectin expression was not affected by metformin treatment.
Conclusion
Metformin treatment improved the increasing effect of lifestyle intervention on the expression of adiponectin receptors in SAT. This effect seems to be achieved through a direct action on SAT.
Conflict of interest: None Disclosed/Payment received. Funding: No Funding/Research realting to this abstract was funded
Obes Facts. 2009 May 14;2(Suppl 2):153–154.
Introduction
Alterations in IGF-1 have been associated with higher prevalence of cardiovascular disease and mortality. While in obese adults low IGF-1 levels have been reported, discordant results are seen in obese children. Accelerated puberty and growth as well as compensatory hyperinsulinemia might be responsible for increased IGF-1 levels in obese children.
Methods
We investigated fasting serum IGF-1, insulin, triglycerides and HDL cholesterol in obese children and adolescents at different stages of pubertal development and assessed the relationship between IGF-1 and the metabolic syndrome parameters, including abdominal circumference and blood pressure. 80 (36 males) obese (BMI SDS>2) prepubertal (59) and pubertal (21) children were studied. IGF-1 was measured by IRMA (DSL) and expressed in SDS for age.
Results
Both IGF-1 and insulin increased with age and pubertal status, but were not correlated. Serum IGF-1, after correction for age, only correlated with diastolic blood pressure (r= −0.264; p=0.028) but not with the other studied variables. IGF-1 SDS levels were comparable between girls and boys (p=0.59) and ranged between −2.28 and +5.03 (median −0.08). IGF-1 SDS increased with advance in puberty (r=0.36; p=0.001), but not with increase in BMI SDS (r=0.09; p=0.44).
Conclusion
Normal IGF-1 levels were seen in obese prepubertal children. Increased IGF-1 levels were observed in late puberty, when compensatory hyperinsulinemia was most marked. The IGF-1 - diastolic blood pressure relationship needs further study in view of later cardiovascular morbidity.
Obes Facts. 2009 May 14;2(Suppl 2):154.
Introduction
Previous studies have shown elevated prolactin (PRL) secretion rates in obese women, in proportion to the size of visceral fat mass. The reduced dopamine D2 receptor-mediated neurotransmission in obese human is one of the proposed mechanisms. Furthermore, adipose tissue has recently been identified as one of the extra-pituitary producing sites of PRL.
Objectives
To analyse the correlation between serum PRL and body mass index (BMI), waist circumference(wc), waist/hip circumferences ratio(wc/hc), and insulinemia in a morbidly obese female population.
Material and methods
107 women were evaluated in their first medical visit for morbid obesity. Anthropometric variables (weight, height, wc, hc) and PRL (mean of values at 0, 20 and 40 minutes) were evaluated. An oral glucose tolerance test was performed, with glucose and insulin determinations at 0,60 and 120minutes. Women under drugs potentially related to hyperprolactinemia were excluded. Results are expressed as mean±standard deviation. Pearson's correlations were used for statistic analysis.
Results
Our population was characterized by: mean age 38.34±11.06; BMI 43.42±7.69Kg/m2; wc 119.77±16.88cm; hc 131.25±15.29cm and PRL 13.90±25.42ng/mL. No statistically significant correlations were found between PRL and any of the analysed parameters (BMI, wc, wc/hc or insulinemia).
Conclusion
Our study was not able to demonstrate a correlation between the mean of a pool of 3 PRL determinations and obesity (namely visceral). Unquestionably, this way of PRL evaluation does not fully illustrate the dynamic of PRL secretion. Whether PRL is synthesized by other adipose deposits beyond the breast, and if its secretion is influenced by obesity, is still a matter of debate.
Obes Facts. 2009 May 14;2(Suppl 2):154.
Introduction
Although it has been shown that visfatin is an adipokine that mimics insulin effect, its implication in glucose homeostasis under different feeding conditions remains controversial. Moreover the effects of functional ingredients, such as conjugated linoleic acid (CLA), on visfatin have not been well established. We aimed to analyze the effects of the trans-10,cis-12 CLA isomer on visfatin under overfeeding and calorie restriction in hamsters.
Methods
8 male Syrian Golden hamsters were fed a standard diet for 7 weeks (C group). 32 hamsters were fed a high-fat diet, supplemented (n=8, HFCLA group) or not (n=24, HF group) with 0.5% trans-10,cis-12 CLA. Control, HFCLA and 8 HF animals were sacrificed. The remaining 16 hamsters were subjected to a 25% calorie restricted diet, supplemented or not with 0.5% CLA (RCLA and RC groups, n=8/group) for 3 weeks. Serum glucose was measured by spectrophotometry, and insulin and visfatin by ELISA. HOMA index was calculated and visfatin expression was measured by RT-PCR in epididymal adipose tissue.
Results
No changes were observed in HOMA index after CLA supplementation under both feeding conditions. With regard to visfatin expression, CLA treatment caused a significant increase in high fat feeding and a tendency to a decrease in energy restriction. These changes in visfatin expression were not paralleled by changes in serum visfatin because this parameter remained unchanged.
Conclusion
Under these experimental conditions, changes in visfatin expression induced by CLA are not associated with changes in insulin sensitivity because HOMA was not modified.
Research funded by Ministerio de Educación y Ciencia (AGL2005-02494); Gobierno Vasco (GIU06/82) and CYTED (208RT0343).
Obes Facts. 2009 May 14;2(Suppl 2):154.
Introduction
CRP has been suggested as a potential cause for human leptin resistance and recently has been shown to affect the relationship between BMI and leptin in a group of men. The purpose of this study was to further investigate this observation in a different study population.
Methods
Blood was obtained from 115 men and women (mean age: 37.70±11.46 years, mean BMI 28.94±4.54) and analyzed for CRP and leptin. Individuals were excluded if they smoked, had heart disease or diabetes, participated in regular physical activity or took medication known to affect CRP levels. CRP levels greater than 10mg/L were excluded from the analysis and log transformed values for CRP and leptin were used when treated as a continuous variable.
Results
CRP and leptin levels correlated significantly (r=0.553, p<0.001) a relationship that was independent of BMI (r=0.425, p<0.001). Both leptin and CRP were related to a range of measures of weight and body composition: Body mass (r=0.255, p<0.01; r=0.306, p<0.01), BMI (r=0.493, p<0.001; r=0.429, p<0.001) and waist circumference (r=0.260, p<0.01; r=0.308, p<0.01). However, while both leptin quartile and CRP quartile were independently related to all measures, the interaction effect was not significant in any analysis.
Conclusion
These data do not support the previously reported theory that high CRP levels are associated with an increase in the observed leptin levels at a given BMI.
Conflicts of Interest: None disclosed. Funding: Research related to this abstracts was funded by NIH, grant 1R15AG#13767-01A1 and a Research Grant from Hartford Hospital. Hartford, USA.
Obes Facts. 2009 May 14;2(Suppl 2):154–155.
Introduction
There is now a substantial body of evidence indicating that bone mass is related to fat mass. However the relationships between body composition, sex hormones, vitamin D status and bone mass still remain controversial. This study aimed to investigate the relative contribution of body composition parameters to bone mass in healthy post-menopausal women.
Methods
We studied 517 postmenopausal women (62.2±6.8 yrs) living in the area of Siena (Italy). In all we measured estradiol (E), sex-hormone binding globulin (SHBG), testosterone (T), 25-hydroxyvitamin D (25OHD), bone alkaline phosphatase (B-ALP), parathyroid hormone (PTH) and carboxy-terminal telopeptide of type I collagen (CTX). BMD was assessed at lumbar spine (BMD-LS), at femoral neck (BMD-FN) and at total femur (BMD-TF). Whole body mineral content (BMC), fat mass (FM), lean mass (LM), android fat (AF) and bone mineral density (BMD) at lumbar spine and femur were assessed by using a DXA device (Lunar GE).
Results
All BMD measurements showed a significant (p<0.001) positive correlation with both FM and LM. E was significantly correlated with fat mass (p<0.05) but not with LM and BMD. However, T was significantly related to femoral BMD (p<0.01) and AF. SHGB was inversely correlated with LM, FM, AF and BMD at all sites. A significant correlation was found between PTH and FM (p<0.05).
Conclusion
Our study suggests that in postmenopausal women FM, LM, T but not E show a positive correlation with BMD. In these subjects body composition seems to be markedly influenced by SHBG, sex hormones and PTH.
Obes Facts. 2009 May 14;2(Suppl 2):155.
Introduction
The aim of the study was to assess the relation of visfatin and insulin in subjects with and without metabolic syndrome.
Methods
The study group involved 92 obese women. On the basis of IDF 2005 criteria the subjects were divided in two subgroups with and without metabolic syndrome (MS). The body mass, height and waist circumference were measured. Plasma concentration of visfatin was measured by ELISA kit, insulin by RIA and glucose and lipids by colorimetric method. HOMA index was calculated.
Results
Higher concentration of insulin was observed in subjects with metabolic syndrome and no differences in visfatin concentrations were detected. However, visfatin/insulin ratio was significantly lower in subjects with metabolic syndrome. Negative correlations of visfatin/insulin ratio with HOMA value were observed in both study subgroups (with MS r = − 0.79, p = 0.0001; without MS r= − 0.71, p=0.0001).
| with MS | without MS | p | |
|---|---|---|---|
| n | 71 | 21 | |
| Age (years) | 52.8±9.4 | 51.7±9.5 | NS |
| Body mass (kg) | 100.9±15.0 | 94.3±13.9 | NS |
| BMI (kg/m2) | 39.1±5.6 | 36.3±5.2 | NS |
| Waist circumference (cm) | 109.6±11.4 | 104.7±11.0 | NS |
| Fat mass (kg) | 52.0±12.8 | 45.2±10.7 | < 0.05 |
| Visfatin (ng/ml) | 33.6±12.6 | 29.8±8.7 | NS |
| Insulin (µIU/ml) | 16.6±10.9 | 8.8±4.6 | < 0.01 |
| Visfatin/insulin | 2.9±2.3 | 3.9±1.5 | < 0.05 |
NS - not significant
Conclusion
We conclude that higher visfatin/insulin index ratio may be one of the counter regulatory factor suppressing development of insulin resistance.
Obes Facts. 2009 May 14;2(Suppl 2):155.
Introduction
Visfatin is a insulinomimetic adipokine. It was also known that adiponectin is a adipokine which increased insulin sensitivity. The aim of the study was to assess the influence of therapy with metformin using on serum concentrations of visfatin and adiponectin in obese women with type 2 diabetes mellitus.
Methods
The study group involved 39 obese women with type 2 diabetes mellitus. After medical history the study group was differentiated to two subgroups: A- treated with use of diet and metformin (age 54.7_±5.9 y, BMI 39.9±5.5 kg/m2) and B - treated use only diet (age 50.9±10.8 y, BMI 40.2±4.6 kg/m2). Blood samples were taken in the morning after an overnight fast. Serum concentrations of visfatin and adiponectin measured by ELISA. Insulin by RIA and glucose by calorimetric methods. HOMA index was calculated with formula.
Results
There were no differences between age and BMI in study subgroups. We did nod observe differences of serum concentrations of visfatin and adiponectin between subgroup A and subgroups B.
| A | B | |
|---|---|---|
| glucose (mg/dl) | 120.1±30.1 | 139.9±33.7 |
| insulin (µIU/ml) | 14.6±9.3 | 23.0±16.2 |
| HOMA | 4.0±2.3 | 8.1±6.1* |
| visfatin (ng/ml) | 33.6±10.8 | 35.4±14.5 |
| adiponectin (µg/ml) | 10.4±3.5 | 10.0±3.8 |
*
p<0.05
Conclusions
Metformin did not influence serum concentrations of visfatin and adiponectin in obese women with type 2 diabetes mellitus.
Obes Facts. 2009 May 14;2(Suppl 2):155–156.
Introduction
Commonly used dietary strategies to prevent osteoporosis have focused on the increased consumption of calcium and vitamin D. However, more recently the dietary acid-base load has acquired an emerging role in the etiology of osteoporosis.
Methods
238 elderly men and women being aged 60-80 years at high risk of cardiovascular disease randomly assigned to three interventional groups, a recommended low-fat diet (control diet group), a Mediterranean diet (Met-diet) supplemented with virgin olive oil or Med-diet supplemented with mixed nuts. Main outcomes were 12-month changes from baseline in bone absorption and resorption markers.
Results
The baseline data on the anthropometric, bone densitometry and biochemical variables did not differ between the three groups. The dietary potential renal acid load (PRAL) and the daily net endogenous acid production (NEAP) at baseline did not differ between groups. After intervention, subjects allocated to the Med-diet supplemented with mixed nuts had a significant increase of PRAL and NEAP. In comparison to the control group and Med-diet supplemented with virgin olive oil group, subjects in the Med-diet supplemented with nuts group had increased parathormone (PTH) levels (+2.63, IC95%:-1.01-6.35, p=0.02) and a non significant increase (+0.31, IC95%:-0.13-0.74, p=0.14) in urine free deoxipiridoline/creatinin ratio (ufDPD/creat), both markers of bone resorption.
Conclusion
The present data suggest that a Mediterranean dietary pattern associated or not to a high dietary acid load derived from consumption of mixed nuts does not seem to have any effect of great magnitude on bone metabolism compared to a control diet in elderly subjects.
Conflict of interest: Dr Jordi Salas-Salvadó is a non payed member of the Scientific Advisory Board of the International Nut Council. The rest of authors have not any conflict of interest affecting the conduct or reporting of the work submitted. Funding: Spanish Ministry of Health, (Instituto de Salud Carlos III, Thematic Network G03/140 and RTIC RD06/0045, Fondo de Investigaciones Sanitarias, PI04/0233, PI04/1828, PI04/2239 and PI05/2368; PI05/1839), CYCYT AGL2005-0365, Public Health Division of the Department of Health of the Autonomous Government of Catalonia, and Fundación Patrimonio Comunal Olivarero and Hojiblanca SA (Málaga, Spain), California Walnut Commission (Sacramento, CA), Borges SA (Reus, Spain) and Morella Nuts SA (Reus, Spain) that donated the olive oil, walnuts, almonds and hazelnuts, respectively, used in the study. None of the funding sources played a role in the design, collection, analysis or interpretation of the data or in the decision to submit the abstract.
Obes Facts. 2009 May 14;2(Suppl 2):156.
Introduction
Dietary fatty acids composition is supposed to change insulin sensitivity. Adiponectin which amount is decreased in obesity, and leptin which level is increased are associated with metabolic phenotypes. The aim of study was to detect influence of 12 weeks of dietary intervention on Lep/Adip ratio in Polish patients with metabolic syndrome (MS).
Methods
55 patients (35-70yrs) with MS were randomized to 4 diets: diet A high fat, SFA-rich; diet B high fat MUFA-rich; diet C low-fat high complex carbohydrate; diet D low fat, high complex carbohydrate diet with 1g/d n-3 PUFA. Fasting leptin (ELISA), adiponectin(ELISA), glucose and insulin (RIA) were measured before and after 12 weeks of diet. The genotyping for SNPs of adiponectin-receptors gene: rs2275737, rs10848571, rs1058322.was performed by RFLP
Results
Decrease of Lep/Adip ratio from 14,1 to 8,5 (p<0,05) in patients on low fat diet enriched with PUFA was observed. No changes in HOMA-IR, HOMA-AD were noticed. The carriers of the measured adiponectin-receptor genes polymorphisms, did not demonstrated differences in HOMA-IR, HOMA-AD as well as Lep/Adip ratio.
Conclusion
Lep/Adip ratio is supposed to be an early sensitive marker of MS metabolic changes. Low fat diet with high PUFA contents seems to be beneficial in preventive strategies non dependently on the investigated adiponectin gene SNPs.
Supported by Lipgene- (Contract FOOD-CT-2003-505944)
Obes Facts. 2009 May 14;2(Suppl 2):156.
Introduction
Menopause-related estrogen deficiency and thyroid disease are associated with cardiovascular disease. The abdominal obesity aggravates this risk. The aim of this study was to assess the relationship between body mass index (BMI) and thyroid-stimulating hormone (TSH) in euthyroid women after bilateral ovarioectomy (BO) and after natural menopause (NM) in the mild iodine deficient region.
Methods
population study of randomly chosen 654 women at the age of 45 − 55 years. Among surveyed two groups were taken out: 120 BO and 108 NM euthyroid women. Difference of age and menopausal duration between groups was not. BMI, waist circumference, TSH were assessed in both groups.
Results
BMI ≥ 25.0 kg/m2 was registered 1.5 times more often in BO than in NM euthyroid women (80.8% vs. 55.6%; p=0.0001). TSH in women after NM with BMI ≥ 25.0 kg/m2 was significantly more than in NM women with BMI < 25.0 kg/m2 (2.0±0.91mU/L vs. 1.6±0.73 mU/L; p=0.02). TSH in women after BO with BMI ≥ 25.0 kg/m2 was 1.9±0.91mU/L and TSH in BO women with BMI < 25.0 kg/m2 was 1.9±0.88mU/L (p>0.05). BMI was positive correlation with TSH in both groups (p>0.05).
Conclusions
TSH and BMI were related in euthyroid women after NM. Probably, increase of TSH can play a role in delay of energy balance and pathogenesis of obesity in women and can be connected with the raised need in thyroid hormones during of menopausal reorganization in conditions of iodine deficiency, especial after BO.
Conflict of Interest: none disclosed. Funding: no funding.
Obes Facts. 2009 May 14;2(Suppl 2):156.
Introduction
There is increasing evidence of higher energy expenditure following protein ingestion as compared to carbohydrates or fat. The mechanisms for the influence of dietary protein on energy expenditure are not clear. It was suggested that proteins and specific amino acids, e.g. leucine, might be involved in the regulation of gene expression and efficiency of ATP production, thus modulating energy balance.
Methods
Male C57BL/6 mice were fed semi synthetic high fat diets containing either 10% or 50% whey protein (WP). A third group was exposed to a 10% WP diet supplemented with L-leucine in a concentration comparable to the 50% whey protein diet. Mice were fed over periods of two or 10 weeks in order to study both short-term and long-term effects. Body weight and food intake were recorded, and body composition measured by quantitative nuclear resonance. Energy expenditure was measured by indirect calorimetry during week 10 of intervention.
Results
10%WP led to significantly increased body weight and fat mass. 50% WP resulted in decreased body weight, body fat mass, and food intake compared to 10% WP. Leucine supplementation mimicked the 50% WP effects only partially.
Conclusion
The potential role of protein in comparison to other macronutrients on energy expenditure and body weight regulation was confirmed. However, further studies are required to elucidate the biochemical mechanisms of action. The results may have an impact in the conservative treatment of overweight and the metabolic syndrome.
Obes Facts. 2009 May 14;2(Suppl 2):156–157.
Introduction
We have recently shown that apelin stimulates glucose utilization in skeletal muscle through an AMP-activated protein kinase (AMPK) dependent pathway. AMPK is also involved in lipid metabolism, activating fatty acid oxidation. So, we studied apelin chronic treatment effects on lipid metabolism in normal and insulin resistant mice.
Methods
Chow fed or high fat fed C57bl6/J mice were ip injected with apelin (0,1µmol/kg/day) during 8 or 28 days. Total [1-14C] palmitate oxidation was determined in soleus muscle as the sum of 14CO2 release and acid soluble metabolites (corresponding to the incomplete oxidation). Intramuscular triglycerides (IMTG) content was measured after extraction of muscle lipids.
Results
Eight days of treatment with apelin decreased perigonadic adipose tissue weight but didn't change neither body weight nor plasma levels of triglycerides and free fatty acids in chow-fed mice. Palmitate oxidation was increased by 68% and IMTG content was decreased by 20% in apelin-treated mice. Similar results were obtained after 28 days of treatment.
In insulin resistant mice, eight days treatment with apelin decreased both perigonadic adipose tissue weight and plasma levels of triglycerides and free fatty acids. Moreover, palmitate oxidation was increased and IMTG content was decreased by 39% in soleus of apelin-treated mice.
Conclusion
By decreasing deleterious lipid accumulation and by stimulating fatty acid oxidation in muscle, apelin chronic treatment could improve insulin resistance.
Obes Facts. 2009 May 14;2(Suppl 2):157.
for the Pennington CALERIE team.
Background
Metabolic (disproportionate lowering of daily energy expenditure) and behavioral (decreased physical activity) adaptations to caloric restriction (CR) in free-living conditions have not yet been objectively measured.
Methods
Forty-eight (36.8±1.0,y), overweight (BMI:27.8±0.7,kg/m2) participants were randomized to four groups for 6-months; Control: 100% of energy requirement; CR: 25% CR; CR+EX: 12.5% CR plus 12.5% increase in energy expenditure by structured exercise; LCD: low calorie diet (890kcal/d) until 15% weight reduction followed by weight maintenance. Body composition (DXA) and total daily energy expenditure (TDEE) over 14-days by doubly labeled water (DLW) and activity related energy activity (AREE) were measured after 3 (M3) and 6 (M6) months of intervention.
Results
At M3, absolute TDEE was significantly reduced in CR (−454±76,kcal/d) and LCD (−633±66 kcal/d) but not in CR+EX or controls. At M6 the reduction in TDEE remained lower than baseline in CR (−316±118 kcal/d) and LCD (−389±124,kcal/d) but reached significance only when CR and LCD were combined (−351±83,kcal/d). Likewise, physical activity (TDEE adjusted for sleeping metabolic rate) was significantly reduced from baseline at both time points. For control and CR+EX, adjusted TDEE (body composition or sleeping metabolic rate) was not changed at either M3 or M6.
Conclusions
For the first time we show that in free-living conditions, CR results in a metabolic adaptation and a behavioral adaptation with decreased physical activity levels. These data also suggest potential mechanisms by which CR causes large inter-individual variability in the rates of weight loss and how exercise may influence weight loss and weight loss maintenance.
Conflict of Interest: The authors have nothing to disclose. Funding: This work was supported by U01 AG20478 (ER). LMR is supported in part by a Neil Hamilton-Fairley Training Fellowship from the NHMRC of Australia (ID 349553).
Obes Facts. 2009 May 14;2(Suppl 2):157.
Because anti-obesity effects of inhibited endocannabinoid signalling might rely on inhibition of hepatic lipogenesis, we hypothesized that CB1 receptor antagonist treatment with SR141716 would be less efficacious in mice feeding an obesogenic diet with lipogenic activity (fish-oil enriched high-fat diet; HF/FO), compared to mice feeding an obesogenic diet with high lipogenic activity (high-fat diet; HF).
Therefore, mice feeding a chow (C), HF or HF/FO diet were orally treated with SR141716 (Rimonabant, mixed in diets), and we compared several aspects of energy balance regulation with non-treated controls. While the HF/FO diet was most obesity-promoting (but with lowest hepatic expression levels of SREBP, ACC and FAS indicating inhibition of hepatic lipogenesis), the weight-reducing effect of SR141716 treatment was largest in the HF/FO group. The HF/FO diet caused obesity without differences in absorbed energy or oxygen consumption. This implies that the rate of oxidative phosphorylation and ATP-production in this group of mice must have been more efficiently coupled than in mice feeding the HF and HC diets. It is speculated that these effects are mediated via increased endocannabinoid signalling, since obesity effects were block entirely with SR141716, again independent of changes in oxygen consumption. Thus, anti-obesity effects of SR141716 treatment occur irrespective of lipogenic activity, and inhibition of hepatic lipogenesis does not seem to play a major role in the anti-obesity effect of SR141716. Furthermore, this study reinforces the idea that endocannabinoid signalling affects metabolic coupling which could play an important role in energy balance regulation.
Obes Facts. 2009 May 14;2(Suppl 2):157–158.
Introduction
Weight loss leads to a reduction in resting energy expenditure (REE) independent of losses in fat-free mass (FFM) and fat mass (FM). We hypothesized that the decrease in specific REE after weight loss is explained by changes in the composition of FFM, i.e. a disproportionate loss in high metabolically active organ mass.
Methods
45 overweight and obese women (BMI 28.7− 46.8kg/m2, 22-46y) followed a 12.7±2.2-wk low-calorie diet. Volumes of brain, heart, liver and kidneys were measured by MRI, skeletal muscle mass was calculated from appendicular lean soft tissue by DXA, FM and FFM were assessed by a four compartment model based on total body water (deuterium dilution), bone mineral content (DXA) and body volume (ADP). REE measured by indirect calorimetry (REEm) was compared to REE calculated from detailed body composition analysis (REEc) using established specific organ metabolic rates.
Results
Mean weight loss was 9.5±3.4kg consisting of 7.8±3.9kg FM and 1.7±3.6kg FFM. There were significant decreases in muscle, heart, liver and kidney masses as well as free triiodothyronine (T3) levels (all P<0.05). After weight loss, REEm adjusted for FFM and FM decreased from 7.33±0.62 to 7.03±0.46MJ/d (P=0.001) and REEm-REEc decreased from 0.78±0.42 to 1.04±0.58 MJ/d (P=0.01). Decreases in REEm adjusted for FFM and FM and REEm-REEc correlated with the drop in T3 (r=0.34, r=0.30, both P<0.05).
Conclusion
Adaptive thermogenesis after weight loss is explained by a reduction in specific organ metabolic rates at a decease in T3 levels, but not by a disproportionate loss in metabolically active organ masses.
Conflict of interest: None disclosed. Funding: Deutsche Forschungsgemeinschaft DFG Mü 714/8-3
Obes Facts. 2009 May 14;2(Suppl 2):158.
As original studies of UCP1-ablated mice failed to demonstrate an obesogenic effect, alternative mechanisms for adaptive adrenergic thermogenesis have been sought. However, we demonstrate here that in C57Bl6 mice exempt from thermal stress (i.e. kept at thermoneutrality), UCP1 ablation in itself induced obesity even in mice fed control diet and vastly augmented diet-induced obesity (high-fat diet), i.e. the mice exhibited increased metabolic efficiency. In wildtype mice, high-fat diet increased norepinephrine-induced thermogenesis, i.e. diet-induced thermogenesis was observed, but no such effect was observed in UCP1-ablated mice, demonstrating that diet-induced thermogenesis fully emanates from UCP1 activity. We conclude that ambient temperature is qualitatively determinative for the outcome of metabolic studies, that no other protein, and no other mechanism, can substitute for UCP1 in mediating diet-induced adrenergic thermogenesis, and that UCP1 activity can be determinative for obesity development in mice, and possibly in humans.
Obes Facts. 2009 May 14;2(Suppl 2):158.
Introduction
Caloric restriction (CR) delays age-related disease and extends lifespan in all studied species. An analysis of many CR studies in rodents suggests that both the degree of CR and the duration of the CR regimen are important. Whether the level of CR is related to changes in biomarkers of longevity, energy expenditure and risk factors for chronic diseases of aging in humans is unknown.
Methods
In the 46 individuals who completed the Pennington CALERIE study we estimated the percent of CR maintained from the intake-balance equation assuming that during CR, energy intake equals energy expenditure plus the changes in energy stores. Energy expenditure was measured by 2-week doubly labeled water and changes in energy stores (fat mass and fat-free mass) were determined by DXA. Pearson correlation analyses were used to assess the degree of CR (% reduction in energy intake from baseline) vs. outcome variables.
Results
At months 3 and 6, the degree of CR was negatively associated with 24h energy expenditure (p<0.00), fasting T3 (p<0.01), total cholesterol (p<0.01), LDL-C (p<0.01), leptin (p<0.01) and ghrelin (p<0.01).
Conclusion
In our 6 month study of CR, part of the inter-individual variability in some of the physiological and behavioral outcomes is associated with the level of CR. An important question is to determine whether these variables are being modulated as a function of weight/ body composition changes independent of CR. Only longer studies with maintenance of weight loss will allow us to disentangle the effect of weight loss vs. CR.
Conflict of Interest: The authors have nothing to disclose. Funding: This work was supported by U01 AG20478 (ER). LMR is supported in part by a Neil Hamilton-Fairley Training Fellowship from the NHMRC of Australia (ID 349553).
Obes Facts. 2009 May 14;2(Suppl 2):158.
Introduction
Large inter-individual differences in adaptive thermogenesis occur when subjects are exposed to mild cold or when they are overfed. These differences are related to mitochondrial uncoupling in skeletal muscle tissue. The objective of this study is to investigate the proteins in muscle tissue that can explain this variation in adaptive thermogenesis.
Methods
The metabolic responses to mild cold and overfeeding in 9 lean adult male subjects were measured in a respiration chamber in a baseline condition, after three days of mild cold exposure, and after three days of overfeeding. After each respiration chamber measurement a muscle biopsy was taken, from which proteins were isolated and separated using 2D electrophoresis. Differentially expressed proteins and proteins linked to energy expenditure were identified using MALDI-TOF-MS/MS.
Results
Eighty-six proteins were differentially expressed and/or their differences in expression correlated to adaptive thermogenesis. Of these 86 proteins, 51 have been identified. Most identified proteins are a part of glycolysis. After overfeeding, the abundance of these glycolytic proteins increased, which indicates a rise in glucose consumption for energy expenditure. Upon mild cold exposure, glycolytic protein abundance decreased, probably because of a larger share of fatty acids in energy metabolism. Nevertheless, upon cold exposure changes in protein expression are positively related to changes in energy expenditure.
Conclusion
This proteomic approach shows a contribution of glycolysis in adaptive thermogenesis. It also suggests that there is a shift in fuel selection between cold and diet induced adaptive thermogenesis.
Conflict of Interest: None Disclosed. Funding: No Funding
Obes Facts. 2009 May 14;2(Suppl 2):158–159.
Introduction
Resting energy expenditure (REE) has been suggested to decrease with age at about 1-2% per decade. Cross sectional data are not ideal to settle the issue, but we were interested in the changes in REE with age in obese women.
Methods
Subjects visited one of three centers in Europe for obesity treatment. Obese females (BMI < 30) were measured for REE with indirect calorimetry. Body composition was measured by bio-impedance (Leuven and Milan), air displacement plethysmography (Amsterdam). Data were retrospectively analysed for age 18-70 years and BMI 30-50. Means are presented with SD. ANOVA with post-hoc Bonferroni has been used for statistical analysis.
Results
In total 835 women were included (402 Leuven, 345 Milan, 88 Amsterdam). Energy expenditure and fat free mass (FFM) decreased with age (both p<0.001). Decrease in REE was about 5% in 4 decades, which is about 100 kcal in 40 years. The change in both REE and FFM was most apparent around 50 years of age. Both obese (BMI 30-39.9) and morbid obese (BMI 40-50) subgroups provided similar results.
| Age (y) | 18-29.9 | 30-39.9 | 40-49.9 | 50-59.9 | 60-69.9 |
| n | 132 | 187 | 216 | 228 | 72 |
| REE (kcal/d) | 1818+255 | 1797+270 | 1813+248 | 1719+247 | 1731+263 |
| FFM (kg) | 52.5+7.1 | 53.2+6.9 | 52.1+6.7 | 48.8+6.0 | 48.2+6.1 |
Conclusion
These cross sectional data show that also (morbid) obese women have a decreased resting energy expenditure with age, which is in line with the suggested 1-2% decrease per decade. A single morbidly obese person can however become more obese over time with no decrease in REE.
Conflict of interest: None. Funding: No funding
Obes Facts. 2009 May 14;2(Suppl 2):159.
Introduction
Anaerobic threshold (AT) and ventilatory compensation point (VCP) are two surrogates of aerobic capacity, so give us information about oxidation rate of fat and carbohydrates during exercise. Training exercise improve VO2 at AT and VCP, which must help to increase energy expenditure during weight loss programs (WLP). Our aim was to analyze the effect of a weight loss program in AT and VCP.
Methods
104 sedentary, healthy, pre-menopausal and, overweight and obese women were included in this analysis (38.6±5.8 yrs; BMI 29.8±3.4 kg.m−2; %FM 46.2±5.2%); A WLP was performed during 10 months. AT and PRC were measured by a breath by breath system using the modified Balke protocol in a treadmill. After WLP the sample was split in three tertiles of weight loss. Repeated measured analysis was performed.
Results
Data shown a reduction in VO2 at AT and VCP in 1st and 2nd tertiles, (AT: 1st 14.2±2.2vs12.9±1.7 ml.kg−1.min−1, 2nd 13.7±2.2vs12.6±1.5 ml.kg−1.min−1,p<0.001 for all; VCP: 1st 19.4±3.2vs18.9±3.0 ml.kg−1.min−1, 2nd 19.1±3.2vs18.5±3.4 ml.kg−1.min−1; p>0.05). However, opposite results were found in 3rd tertile of VCP (18.5±2.9vs20.2±4.2 ml.kg−1.min−1,p<0.01), and none change o AT (p>0.05).
Conclusions
The main finding of this study was a reduction on aerobic capacity after weight loss. Changes on body composition must be in origin of these relationships. However, women with higher reductions shown an opposite effect, which can be result from an increase on exercise of high intensity and volume. More research is needed to fully understand this relationship.
Obes Facts. 2009 May 14;2(Suppl 2):159.
Introduction
Green tea (epigallocatechin gallate+caffeine), and protein each have been shown to improve body weight maintenance after weight loss. Therefore, the effect of a Green tea-caffeine mixture added to a relatively high-protein diet, on weight-maintenance after body-weight loss in moderately obese subjects was investigated.
Methods
A randomized placebo-controlled double blind parallel trial in 80 overweight and moderately obese subjects, (age: 44±2yrs; BMI: 29.6±2.0 kg/m2) matched for gender, age, BMI, height, body-mass and with a habitually low caffeine intake. A very low energy diet intervention during 4 weeks was followed by 3 months weight-maintenance (WM); during the WM period the subjects received a green tea-caffeine mixture (270 mg epigallocatechin gallate+150 mg caffeine/day), or placebo, both in addition to a just adequate protein diet (AP: 50-60g protein/day) vs. a high protein diet (HP: 100-120g protein/day).
Results
Subjects lost 7.0 kg±1.6 (SD), or 8.2%±2.0 (SD) body-weight (p<0.001). During the weight-maintenance phase, weight-maintenance, REE, fat free mass (FFM) were relatively increased, in both the HP groups and in the Green tea-caffeine mixture group+placebo (p<0.05), while RQ and body-fat (FM) were reduced, all compared to the AP+placebo group. Satiety was only increased in both HP groups (p<0.05). The Green tea-caffeine mixture was only effective in the AP diet.
Conclusion
Green tea-caffeine mixture, as well as a high-protein diet each improved weight-maintenance independently, through thermogenesis, fat oxidation, sparing fat free mass, and for the high-protein diet through satiety; a possible synergistic effect failed to appear.
Conflict of interest: No conflict of interest. Funding: Nutrim, Maastricht University and Novartis Nutrition Nyon
Obes Facts. 2009 May 14;2(Suppl 2):159.
Introduction
Equations to predict resting metabolic rate (RMR) in obese subjects with poorly controlled type 2 diabetes (T2DM) have not been identified.
Methods
In an ongoing randomized trial, obese subjects (BMI ≥ 30kg/m2) with poorly controlled T2DM (HbA1c ≥ 7.5%) were recruited. Their RMR was measured by indirect calorimetry using the Quark RMR (Cosmed, Italy) and compared to 27 predictive equations. The accuracy of equations was assessed by the percentage of subjects who's estimated RMR fell within 10% of the measured RMR (mRMR) and the bias between the predicted and mRMR (mean percentage difference).
Results
39 subjects were recruited (16 males: 23 females); BMI range 30–52 kg/m2 (mean: 38.6, SD: 5.8); age range 37–75 y (mean: 56.6, SD: 10.1); HbA1c range 7.5–12.3% (mean: 8.9, SD: 1.3), mRMR range 1128–3345 kcal/d (mean: 1988, SD: 427). The most accurate estimation of RMR was obtained using the Lazzer equation (precision accuracy: 59%; bias: −2.43%). When selected for BMI, RMR for subjects with BMI < 35 kg/m2 (n=27) was most accurate using the WHO equation (precision accuracy: 51.8%; bias: −5.17%) while for a BMI ≤ 35 (n=12) the Mueller equation was most accurate (precision accuracy: 66.7%; bias: 0.68%).
Conclusions
For obese individuals with poorly controlled T2DM the Lazzer equation was the most accurate, however a precision accuracy of 59% is far from ideal. Despite the small sample size, we suggest that there is currently no accurate equation available to predict RMR in obese patients with poorly controlled T2DM.
Conflict of interest: None disclosed. Funding: The studentship of a research student (AG) was funded by the Go Lower
Obes Facts. 2009 May 14;2(Suppl 2):159–160.
Introduction
Fatty Acids (FAs) are an important source of energy. FAs differ by chain length, double bond and its position. Saturated FAs (SAFAs) are known to increase the risk of CHD by elevating the values of LDL-cholesterol. Mono unsaturated FAs (MUFAs) have an effect of vascular protection and poly unsatured FAs (PUFAs) are precursors of the eicasonoids.
Methods
Patients were grouped according to gender and BMI (group 1: BMI ≥ 40, group 2: BMI < 25, group 3: BMI < 40). Patients in group 1 (22 females, 12 males) received bariatric surgery while patients in group 2 (14/14) and group 3 (18/14) underwent a necessary surgical procedure. FAs were ascertained in plasma, subcutaneous and visceral adipose tissue.
Results
Significant gender specific differences were found in plasma, subcutaneous and visceral adipose tissue. In females and males there were significant differences in 18:0 und 18:1ω7 between the groups in subcutaneous and visceral adipose tissue, which are, for females, partially reflected in plasma. There are significant differences between the groups for PUFAω-3 in both sexes.
Conclusion
It is well known that the pattern of FAs depends on the food supply. When comparing the FA pattern in plasma with the two tissue compartments there are different correlations. One reason for the disparity could be that FAs in plasma are transported in triglycerides, cholesterol and phospholipids. Further studies are needed to elucidate the causal relationship.
Conflict of Interest: None: Funding: No Funding
Obes Facts. 2009 May 14;2(Suppl 2):160.
Introduction
Studies on chilli peppers have shown positive effects on energy intake (EI) and meal-induced thermogenesis (MIT), but there are few studies of other pungent spices. The present study examined the acute effects of black pepper (pepper), ginger, horseradish and mustard on subjective appetite measures, ad libitum EI and MIT.
Methods
In a 5-way placebo-controlled single-blinded crossover trial 22 healthy, young (age: 24.9±4.6 years, mean±SD), normal weight (BMI: 21.8±2.1 kg/m2) males were randomly assigned to receive a brunch meal with either pepper (1.3 g), ginger (20 g), horseradish (8.3 g), mustard (21 g) or no spices (placebo).
Results
Mustard produced a MIT of 235±10 kJ/4h (mean±SE), which tended to be larger than the MIT of placebo (14%, 206±9 kJ/4h, p=0.083), and was 20% larger than the MIT of ginger, horseradish and pepper (range: 184-195±8-10 kJ/4h, p<0.023).
No differences were observed in fat oxidation (p=0.17), carbohydrate oxidation (p=0.31), respiratory quotient (RQ) (p=0.73) or catecholamine levels (p>0.50).
Horseradish decreased heart rate vs. both placebo and mustard (p<0.049). Diastolic blood pressure increased following horseradish intake vs. both placebo (p=0.049) and pepper (p<0.001), and non-significantly vs. ginger (p=0.050). Systolic blood pressure did not differ between treatments (p=0.15).
No effects were seen on subjective appetite measures (p>0.86) or ad libitum EI (p=0.62).
Conclusions
Mustard tended to be thermogenic at the given dose without causing any side effects. More studies are needed to examine this and other effects of the spices further and elucidate the possible mechanisms.
Conflict of interest: None disclosed/The authors declare no conflict of interest. Funding: The study was funded by the Programme Commission on Health, Food and Welfare (the Danish Council for Strategic Research). Author NTG is supported by a research grant from Unilever.
Obes Facts. 2009 May 14;2(Suppl 2):160.
Introduction
Different outcomes over the effect of green tea on weight loss and weight maintenance have been reported in studies with Asian subjects compared to Caucasian subjects. By conducting a meta-analysis the question whether or not green tea indeed plays a role in body weight regulation can be elucidated.
Methods
English language studies and references from the retrieved articles were found in PubMed to identify studies about weight loss (WL) and weight maintenance (WM) after green tea supplementation (GT), to use in this meta-analysis. Initially 48 studies were retrieved and after an extensive selection this was brought down to 11 articles. Effect sizes (yi) were computed and the yi values were aggregated based on a random-effects model, using restricted maximum-likelihood (REML) estimation to estimate the amount of heterogeneity in the effect sizes.
Results
Catechins significantly decreased body weight and significantly maintained body weight after a period of weight loss (d=0.148; p<0.01). Also, high habitual caffeine intake (>300 mg/d) prevents the effect of catechins on body weight (d=0.122; p<0.05). Furthermore, the effect of catechins is less in Caucasian subjects compared to Asians (d=0.142; p<0.01).
Conclusions
Catechins or an EGCG-caffeine mixture have a positive effect on weight loss and on weight maintenance. Habitual caffeine intake and ethnicity are important moderators.
Conflict of interest: No conflict of interest. Funding: Nutrim, Maastricht University
Obes Facts. 2009 May 14;2(Suppl 2):160.
Introduction
Atenolol is a specific beta-1 adrenergic receptor blocker commonly prescribed for the treatment of hypertension. Weight gain and hyperglycemia are common side-effects which are partially mediated through alteration of adipose tissue metabolism. These side-effects are particularly concerning for populations, such as type 2 diabetics.
Objective
We sought to determine how atenolol affects adipose tissue function in type 2 diabetic men during exercise. Specifically, we evaluated how atenolol affects adipose tissue secreted hormones such as acylation stimulating protein (ASP) which plays a role in adipose tissue fatty acid metabolism.
Methods
Ten type two diabetic men underwent a one-hour exercise session at 60% of their V02max under four different conditions: 1) fasting after one week treatment with atenolol or 2) with placebo; and 3) two hours postprandial with placebo or 4) after one week treatment with atenolol. In addition, we also evaluated the direct effects of atenolol and the non-specific beta-blocker propranolol on adipocyte function using the 3T3-L1 murine adipocyte cell model.
Results
There were no changes in weight, HbA1c, or fasting glucose with atenolol treatment. Treatment with atenolol decreased circulating ASP in type 2 diabetic men; however, ASP did no change as a result of exercise or under postprandial versus fasting conditions. We then went on to test if the effects of atenolol on ASP production were direct or indirect. Treatment for 48 hours with 10nM atenolol did not change ASP production by 3T3-L1 adipocytes but did prevent epinephrine-mediated decreases in ASP production.
Obes Facts. 2009 May 14;2(Suppl 2):161.
Lifestyle changes can successfully induce weight loss in obese individuals, at least temporarily. But there is presently no way to quantitatively estimate the permanent changes of diet or physical activity required to prevent weight regain. Such a tool would be helpful for goal-setting since obese patients and their physicians could assess whether adherence to the calculated lifestyle change is realistic. To address this issue, we developed a mathematical model to calculate the body weight change arising from a given energy intake change, and conversely, the modification of energy intake required to maintain a particular body weight change. We used data from 8 longitudinal weight loss studies representing 157 subjects with initial body weights ranging from 68-160 kg and stable weight changes between −7 and −54 kg. Model calculations closely matched the weight change data (R2 = 0.83, χ2=2.1, p < 0.01 for weight changes, R2 = 0.91, χ2= 0.87, p < 0.0004 for energy intake changes) and also accurately predicted the proportion of weight change resulting from the loss of body fat (R2 = 0.90). Therefore, our model provides the first realistic calculations of lifestyle modifications required for weight loss maintenance. Standard spreadsheet files of the model can be freely downloaded at http://www2.niddk.nih.gov/NIDDK-Labs/LBM/lbmHall.htm and can therefore be widely used by physicians and weight management professionals.
This research was supported by the Intramural Research Program of the NIH, NIDDK.
Obes Facts. 2009 May 14;2(Suppl 2):161.
Introduction
We aimed to assess the expression patterns of lipogenesis-and lipolysis-related genes in white adipose tissue (WAT) and liver after carbohydrate (CH) or fat (F) feeding.
Methods
Adult male Wistar rats were studied under 24h fasting conditions and after 24h fasting followed by a 12h re-feeding period with 64Kcal of CH or F, consisting in a mixture of wheat starch and sucrose or bacon, respectively. The expression (by RT-qPCR) of selected genes involved in lipid metabolism in WAT and liver was analysed.
Results
In WAT, CH re-feeding increased the expression of genes related with lipogenesis (PPARgamma, GLUT4, Hexokinase) and lipolysis (HSL and AGTL). However, after F re-feeding, the expression of some lipogenesis-related genes (PPARgamma, GLUT4, Hexokinase) remained unchanged, while others (FAS, CD36, LPL) decreased. In liver, CH re-feeding increased the expression of lipogenesis-related genes (FAS, Glucokinase, SCD1, SREBP1c), and inhibited the expression of CD36 and of fatty acid oxidation-related genes (PPARalpha, CPT1-L, PDK4). F re-feeding did not increase the expression of lipogenesis-related genes, while increased the expression of genes related with fatty acid oxidation. Moreover, liver triglyceride content increased after F re-feeding but not after CH re-feeding.
Conclusions
These results show differences in the expression of genes involved in fuel handling and partitioning after CH or F intake, that may result in increased fatty acid oxidation and triglyceride storage in liver after F feeding, and a less efficient storage of F in WAT, can explain the known effects of high-F diets to promote pathological features of the metabolic syndrome.
Conflict of interest: None Disclosed. Funding: Research relating to this abstract was funded by the Spanish Government (grant AGL2006-04887/ ALI). The CIBER de Fisiopatología de la obesidad y nutrición is an initiative of the ISCIII.
Obes Facts. 2009 May 14;2(Suppl 2):161.
Metabolizable energy in rodent diets are often estimated by Atwater factors (protein/carbohydrate 4 kcal/g, fat 9 kcal/g). This implies nutrients and energy digestibilities above 90%. We experimentally determined digestibility of energy (DoE) and protein, and nitrogen balance. Body-weight (BW) gain and body composition in pair-fed Wistar rats (isocaloric amounts of two different low-carbohydrate/high-fat diets LC-HFD-1:fat~66%ME and LC-HFD-2:fat~94%ME; carbohydrates~1%ME) in comparison to rats fed regular Chow (CH:fat~9%ME) were analysed.
Results
After 4 weeks on the respective diets, area under the curve for BW development was lower in LC-HFD groups (CH: 1472±319, LC-HFD-1: 1046±259; LC-HFD-2: 414±147; CH vs. LC-HFD-1 and LC-HFD-2: p<0.01). LC-HFD groups had significantly more body fat and higher serum leptin levels. DoE increased for both LC-HFD compared to CH (CH: 75.9±3.1%; LC-HF-1: 91.9±2.7%; LC-HF-2: 91.9±5.1%; CH vs. HF-LC-1 and −2; p<0.001). Protein digestibility was about 30% higher in both LC-HFD groups (p<0.001). LC-HFD-1 fed rats accumulated most nitrogen/day; LC-HFD-2 the least. Nitrogen balance was positive in all groups. DoE estimations by Atwater were imprecise for LC-HFD-1, but adequate for CH and LC-HFD-2, whereas protein digestibility was overestimated in all three diets.
Conclusion
Experimental re-evaluation of digestibility seems necessary when experimental settings require exact knowledge of dietary energy contents. The low protein content in LC-HFD-2 (~5%ME) was sufficient to sustain a positive nitrogen balance, but might be insufficient for physiologic growth, e.g. muscle mass acquisition - a factor that should be kept in mind, when working with LC-HF diets and a potential explanation for the impaired BW gain in LC-HFD-2.
Obes Facts. 2009 May 14;2(Suppl 2):161–162.
Introduction
Oleoyl-estrone (OE) lowers body fat mainly by decreasing lipogenesis and fatty acid incorporation in WAT. Beta-3 agonist CL316,243 (B3A) increases lipid mobilization. Combination of OE+B3A results in an additive loss of body fat, but the mechanist of this synergy is not known.
Methods
Adult overweight male rats were treated for 10 days with oral 10 nmol/g OE, and constant subcutaneous infusion of B3A (1mg/kg·day). Whole epididymal, inguinal-subcutaneous, and retroperitoneal fat pads were used for the estimation of cAMP and the expression of lipogenic, lipolytic enzymes, lipoprotein lipase (LPL) and GLUT4
Results
OE did not change the concentrations of cAMP in WAT sites nor the expression of lipolytic enzymes, but decreased the expression of fatty acid synthesis enzymes, LPL and GLUT4. B3A increased cAMP and all expressions. Combination of OE+B3A resulted in different effects depending on the site, but in general the expressions were hardly different from controls.
Conclusion
The opposing effects of OE on fatty acid synthesis and their different action on lipolysis and import of glucose and lipoprotein-derived fatty acids are clearly apparent, however, their combined action results in a synergistic loss of fat despite much less marked changes in enzyme expressions; however, cAMP levels in the tissue are better correlated with the overall loss of fat, suggesting that this is the key factor in the control of WAT fat content.
Conflict of Interest: None Disclosed. Funding: Grant SAF2006-05134 of the Government of Spain. And CIBER Obenutr, a ISCIII initiative.
Obes Facts. 2009 May 14;2(Suppl 2):162.
Introduction
Chronic oleoyl-estrone (OE) treatment induces transient increases in circulating corticosterone and ACTH in rats, and favour hepatic conversion of dehydrocorticosterone to corticosterone, thus increasing the overall availability (and probably effects) of the hormone. We studied here whether the adrenals’ response to OE also favours high corticosterone levels.
Methods
Adult overweight male rats were treated for 10 days with oral 10 nmol/g OE and compared with controls and a pair-fed group. Adrenal glands were dissected and used for analysis of the expression of the corticosterone synthesis enzyme genes. Plasma was used for the measurement of corticosterone and dehydrocorticosterone levels through derivatization and HPLC-MS/MS analysis.
Results
Adrenal gland weight increased in OE versus controls and pair-fed. OE and pair-feeding increased circulating corticosterone levels but left dehydrocorticosterone unchanged. OE increased the gene expression of the enzymes/complexes related to the uptake of cholesterol and its conversion to pregnelonone, and the conversion of progesterone to corticosterone, but lowered 11beta-hydroxysteroid dehydrogenase1. Pair-feeding decreased the conversion of cholesterol to progesterone but increased 11beta-hydroxylase.
Conclusion
OE increased the ability of the adrenal glands to synthesize corticosterone (larger size, cholesterol uptake and increased enzyme expressions), an effect not due to limited food intake (pair feeding had no comparable actions). Increased levels of corticosterone may be in part due to increased adrenal production (OE) or reconversion from dehydrocorticosterone in other tissues (pair-fed).
Conflict of Interest: None Disclosed. Funding: Grant SAF2006-05134 of the Government of Spain. And CIBER Obenutr, a ISCIII initiative.
Obes Facts. 2009 May 14;2(Suppl 2):162.
Introduction
Aim of this study was to describe the effect of a change in dietary fat intake on body weight, variation in blood lipids and hormonal levels.
Methods
366 adult participants (BMI 34.2±4.9 kg/m2, age 42.4±6.1 yr) underwent 8 months of weight management. After 8-week LCD (low calorie diet) they were instructed to follow a low fat diet. Anthropometric parameters (weight, height, waist and hip circumference, sagittal diameter), parameters of lipid metabolism and adiponectin were measured before the start of LCD diet, after LCD and at the end of the study. The subjects were divided into groups according to change of their fat intake (DF decrease in fat intake more than 20 g/day, NCF no change or higher fat intake) in comparison with initial diet.
Results
The average BMI change was −3.7±2.4. There were no significant correlation between fat intake and change of BMI during study and with change of adiponectin level. We found effect of low fat diet on decrease of total cholesterol level. This decrease was in both HDL (p=0.06) and LDL (p=0.06) cholesterol. We also found increased levels of triglycerides in group with lower fat intake (p=0.07).
Conclusion
We found no significant correlation between fat intake and changes of BMI and adiponectin levels. Lower dietary fat intake led to higher decrease of total, HDL and LDL cholesterol levels. We also found lower triglyceride levels in groups with higher fat intake.
Conflict of Interest: None Disclosed. Funding: Supported by the European Community (Contract no. FP6-513946), http://www.diogenes-eu.org
Obes Facts. 2009 May 14;2(Suppl 2):162.
Introduction
Oleoyl-estrone (OE) is a natural steroidal hormone ester with a powerful ability to reduce the body weight in a number of rat obesity models and diabetes and in genetically obese ob/ob and db/db when administered intravenously. Here, we assess the effects of oral administration of OE in a dietary model of obese mice.
Methods
Male mice were fed for 8 weeks with standard pellet (STD) or a cafeteria diet (KAF). Then, each group was subdivided in four and submitted to a daily gavage of vehicle or OE (0.01, 0.05 and 0.150µmol/kg/day) for 10 days. Tissues were weighted and serum metabolites were determined.
Results
KAF mice showed an increase in body weight of 59% in 8 weeks whereas standard diet promoted a weight growth of 28%. Obese mice increased adipose tissue weight (BAT, perigonadal, retroperitoneal, subcutaneous and mesenteric) between 2 and 4 times, being the retroperitoneal the more affected depot. Serum glucose, total cholesterol and triglycerides were statistically increased and urea decreased in KAF mice. Oral OE elicited a dose-dependent loss of body weight in KAF whereas STD did not modify it. KAF reduced adipose tissue mass of all depots and normalized circulating cholesterol, glucose and triglycerides. Retroperitoneal and epididimal WAT were also reduced in STD mice and glucose the only metabolite sensitive to OE. Testicle size was totally unaffected by OE treatment.
Conclusion
In mice with obesity induced by a cafeteria diet, oral OE is able to reduce all the adipose depots and normalize disturbed lipemia and glucemia.
Conflict of interest: None Disclosed. Funding: Grant SAF2006-05134 of Governament of Spain. And CIBER Obenutr, a ISCIII initiative.
Obes Facts. 2009 May 14;2(Suppl 2):162–163.
Introduction
In this study we evaluate the effect of high fat diet rich in lard or fish oil on both total body and mitochondrial energy efficiency.
Methods
Three groups of rats were used: control rats receiving standard diet (N), rats receiving an high fat diet rich in lard (40% J/J) (L), rats receiving an high fat diet rich in fish oil (40% J/J) (FO). The experimental period lasted 6 weeks. Total body oxygen consumption, body composition and energy efficiency, energy balance analysis, serum triglycerides and cholesterol levels, oral glucose tolerance test, and liver lipid content were determined. Hepatic mitochondrial energy efficiency was determined by measuring basal and fatty acid induced proton leak kinetics.
Results
Body weight and lipid gains, triglyceride and cholesterol serum levels, hepatic lipid content, and insulin response to oral glucose load were lower in FO than in L rats. The percentage of metabolizable energy intake stored as lipid was greater in L than in FO rats. FO rats exhibited the higher body oxygen consumption. Body energy efficiency increased in L rats compared to N ones and decreased in FO rats compared to L ones. Compared to N rats, L rats showed a decreased fatty acid induced proton leak. FO rats exhibited an increased basal and fatty acid induced proton leak.
Conclusions
In chronic overnutrition, high fat diet rich in fish oil, compared to high fat diet rich in lard, reduced glucose dependent insulin secretion, adiposity and ipertriglyceridemia by decreasing total body and mitochondrial energy efficiency.
Conflict of Interest: None disclosed. Funding: No funding
Obes Facts. 2009 May 14;2(Suppl 2):163.
withdrawn
Obes Facts. 2009 May 14;2(Suppl 2):163.
Introduction
Treatment of morbid obesity with diet/exercise is ineffective. Epigenetic factors may play a role in promoting the massive obesity seen in some individuals. The most successful treatment for morbid obesity is biliopancreatic diversion (BPD) bariatric surgery.
Objective
To investigate the impact of morbid obesity and subsequent weight loss via BPD surgery on children born before maternal surgery (BMS) and after maternal surgery (AMS).
Methods
Forty-five women who had undergone BPD weight loss surgery at Hôpital Laval and had children born before BPD, after BPD, or both were recruited with their children to participate. Fasting blood samples and anthropometric measurements were collected for both mothers and children. A medical history questionnaire was also completed. Blood samples were analyzed for lipids, glycemia, and adipose-tissue secreted hormones (adipokines).
Results
BMS children (n=50) had a higher rate of overweight and obesity (defined using age-adjusted cut-points, to correct for age differences), higher waist circumference and a higher body fat percentage than AMS (n=52) children. Further, BMS children had higher glucose, triglyceride, LDL cholesterol, C-reactive protein, insulin and leptin, and lower HDL cholesterol and ghrelin. The incidence of complications during pregnancy (such as preeclamspia, and gestational diabetes) decreased as a result of BDP.
Conclusion
Intrauterine environment may play an important role in determining susceptibility for obesity. The positive health implications of BPD may extend beyond the mother's health to future generations.
Conflict of Interest: None Disclosed. Funding: This work was supported by Canadian Institutes of Health Research (KC).
Obes Facts. 2009 May 14;2(Suppl 2):163.
Introduction
Perinatal factors may affect the susceptibility to suffer from obesity and metabolic alterations in adulthood. Here, we aimed to assess the effects of caloric restriction in lactating rats on later body weight and insulin sensitivity of their offspring.
Methods
Lactating Wistar dams were fed with either ad libitum standard diet or a 30% caloric restricted diet throughout lactation. After weaning, the offspring were fed with a normal-fat (NF) diet until the age of 15 weeks, and then with a NF or a high-fat (HF) diet until the age of 28 weeks. Body weight and food intake was followed. Plasma glucose and insulin were measured under different feeding conditions (ad libitum, 14h fasting and 3h refeeding after 14h fasting) and at different ages.
Results
The offspring of caloric restricted dams (CR) had lower body weight than the offspring of controls (C), and were also more resistant to the weight gain and fat accumulation occurring under HF diet, particularly in male animals. CR also ate fewer calories than their controls. In addition, both male and female CR displayed lower insulin levels than C under different feeding conditions, and, in males, the HOMA-IR was significantly lower. Moreover, CR were protected against the increase in HOMA-IR occurring in male rats under HF diet.
Conclusion
These results indicate that a moderate caloric restriction during lactation could be protective from obesity development in the offspring in adult life and from metabolic related alterations, particularly insulin resistance, associated to an HF diet feeding.
Conflict of interest: None Disclosed. Funding: Research relating to this abstract was funded by the Spanish Government (grant AGL2006-04887/ ALI). The CIBER de Fisiopatología de la obesidad y nutrición is an initiative of the ISCIII.
Obes Facts. 2009 May 14;2(Suppl 2):163.
Introduction
As with weight loss after gastric resection, there may be many causal factors including food intake and gastrointestinal hormones. Therefore, we evaluated prospectively changes in appetite, body composition, body weight, ghrelin and PYY3–36 to elucidate the association of gastrointestinal hormones with weight loss after gastric resection.
Methods
We measured appetite score and nutrition intake in 18 patients with early gastric cancer (EGC, mean age; 56 yrs) before and 1 year after gastric resection. Blood samples for ghrelin, PYY3–36 as gut hormones were collected from all patients before, 1 hour, 1, 3, 7 days and 1 year after surgery.
Results
All subjects had lost their weight on the follow-up. Of the 18 subjects, 11.1%, 55.5%, and 33.3% lost < 5%, 5-10%, and < 10% of baseline body weight about 1 year after surgery, respectively. The ghrelin concentration decreased to 42.8% of preoperative levels at 1 hour, then gradually increased to 85.8% by 7 day, and finally reached to 58.7% at 1 year after surgery. Mean weight and percentage body fat loss were 10.3% and 23.9%, relative to initial measurements. There was no change in appetite, nutrition intake and PYY3–36 during 1year.
Conclusions
Weight and percentage body fat loss in patients with EGC who underwent gastric resection is associated with decreased ghrelin concentration by surgery without changes in appetite and nutrition intake.
Conflict of Interest: None. Funding: supported by Medical Research Institute Grant (2005-01), Pusan National University
Obes Facts. 2009 May 14;2(Suppl 2):164.
Introduction
The protein leverage hypothesis suggests that energy intake is adjusted to maintain a protein intake target.
Methods
6 lean, healthy females were housed for 4 days on 3 occasions. On each occasion they had either a 10% (10% P, 60% CHO, 30% fat), 15% (15% protein, 55% CHO, 30% fat) or 25% (25% protein, 45%, CHO, 30% fat) protein diet, with each subject receiving all three diets across the study in random order. These diets were covertly manipulated to be similar in variety, energy density and palatability. Ad libitum energy intake (EI) was measured over each 4 day period. Energy intake for days 3 and 4 for each participant on each occasion was ranked 1 (lowest) to 3 (highest) with respect to %P.
Results
One subject was excluded from the analysis due to illness at the beginning of one study week. The mean total EI over the 4 days was 36.2±2.8, 35.0±3.5 and 33.4±2.3 MJ for the 10%, 15% and 25% protein diets respectively. Although mean total EI for days 1 and 2 did not differ between diets (17.3±1.4, 17.5±1.4 and 17.2±1.2 MJ, for the 10, 15 and 25% protein diet respectively), a difference was apparent for days 3 and 4, where intake was 18.9±1.6, 17.5±2.0 and 16.2±1.1 MJ for the 10, 15 and 25% protein diet respectively. Intake within subjects on days 3-4 consistently ranked lowest on 25% and highest on 10% protein diets, and was significantly higher on the 10% than the 15% (1.8, p = 0.03) and 25% (1.4, p = 0.004) protein diets.
Conclusion
Altering the percentage protein in the diet leads to a significant change in energy intake after 2 days of feeding, supporting the protein leverage hypothesis.
Conflict of Interest: None Disclosed. Funding: Research relating to this abstract was funded by NH&MRC of Australia
Obes Facts. 2009 May 14;2(Suppl 2):164.
Introduction
Olanzapine (OLZ) is an a-typical drug for treatment of schizophrenia. It also causes weight gain, insulin resistance and increased risk for development of diabetes. In contrast, the anti-convulsant, Topiramate (TPM), has the capability to improve insulin/glucose sensitivity and reduces weight. We use these two drugs to investigate the underlying mechanisms of drug-induced diabetes and weight alterations.
Method
Rats were equipped with a gastric cannula for drug administration and a jugular vein cannula for blood sampling during an intra gastric glucose tolerance test (IGTT). The animals were given a palatable medium fat diet and housed in cages that allow measurements of sponteanous home cage and running wheel activity. OLZ or TPM were chronically administered for a period of at least 3 weeks. IVGTT's were given before and after treatment. Body fat distribution and carcass analysis were performed at the end of treatment.
Results
TPM immediately increases insulin sensitivity and improves glucose clearance during an IGTT. It also leads to a reduction in weight and body fat percentage. Chronic OLZ treatment markedly reduced spontaneous activity but failed to have an effect on food intake, body weight and glucose levels.
Discussion
Both OLZ and TPM act on several levels of the body. TPM markedly improves glucose tolerance and insulin sensitivity, in part through its action on the central nervous system and partly through its effect on muscle and fat. Chronic administration of OLZ seem to cause only minor changes, however we recently found a more effective route of intragastric administration.
Conflict of Interest: None Disclosed. Funding: Research relating to this abstract was funded by Top Institute Pharma project T2-105.
Obes Facts. 2009 May 14;2(Suppl 2):164.
Introduction
Leptin and ghrelin are known to be main hormones involved in the control of food intake, with opposite effects. Here we aimed to assess whether changes in leptin and ghrelin systems are involved in the different satiating capacity of carbohydrates (CH) and fat (F).
Methods
Adult male Wistar rats were studied under 24 h fasting conditions and after 24 h fasting followed by a 12 h re-feeding period with 64 Kcal of CH or F, consisting in a mixture of wheat starch and sucrose or bacon, respectively. Serum levels of leptin and ghrelin, and mRNA levels of leptin (in the retroperitoneal adipose tissue) and NPY and POMC (in the hypothalamus) were measured.
Results
CH re-feeding resulted in higher leptin mRNA expression levels in the adipose tissue and in higher circulating leptin levels compared with those after F re-feeding. Moreover, the ghrelin/leptin ratio was significantly higher after F re-feeding compared with CH re-feeding. Expression levels of hypothalamic neuropeptides involved in food intake control and regulated by these hormones, particularly the orexigenic NPY and the anorexigenic POMC, were also differently affected by CH and F re-feeding, resulting in an NPY/POMC ratio significantly lower after CH re-feeding than after F re-feeding.
Conclusion
Different effects on the leptin and ghrelin systems can account, at least partially, for the lower satiating capacity of F compared to CH.
Conflict of interest: None Disclosed. Funding: Research relating to this abstract was funded by the Spanish Government (grant AGL2006-04887/ ALI). The CIBER de Fisiopatología de la obesidad y nutrición is an initiative of the ISCIII.
Obes Facts. 2009 May 14;2(Suppl 2):164–165.
Introduction
Understanding the mechanism behind food intake and energy expenditure is important for the treatment of obesity. Acylation stimulating protein (ASP, C3adesArg) is an adipokine which stimulates triglyceride synthesis and glucose transport via interaction with its receptor C5L2. This receptor is expressed peripherally (adipose tissue, muscle) and centrally. Previous studies have shown that ASP-deficient mice (C3KO) and C5L2-deficient mice (C5L2) are hyperphagic (59% to 229% increase, P < 0.0001) counter-balanced by increased oxygen consumption (VO2) and a lower RQ.
Objectives
Elucidate the ASP-C5L2 pathway in the brain by assessing the central effect of ASP on food intake, energy expenditure and neuropeptide expression.
Methods
Male Rats were surgically implanted with intracerebroventricular (i.c.v.) cannulas directed towards the third ventricle. After a 5 hr fast, rats were injected. Food intake was assessed at intervals of 0.5, 1, 2, 4, 16 and 24 hr. Body weight was measured pre-injection and after 24 hours. There was a 5-7 day washout period between each injection. For energy expenditure assay rats were housed in a calorimetric chamber for 48 hours before injection.
Results
We observed that acute i.c.v. injections of ASP have a dose dependent effect on food intake. ASP injection interestingly diminishes food consumption by 20% to 50% (P< 0.05) at according to time and concentration over a 24 hour span. Furthermore, acute ASP injection affected energy substrate usage demonstrated by a lower RQ, and affected movement with a 49% decrease in total activity but there was no change in oxygen consumption (VO2).
Conflict of Interest: None to disclose. Funding: Research relating to this abstract was supported by the Canadian Institutes of Health Research.
Obes Facts. 2009 May 14;2(Suppl 2):165.
Introduction
Leptin is an adipokine that regulates energy metabolism. We have previously shown that leptin inhibits food intake by suppressing the activity of AMP kinase (AMPK) in the arcuate (ARH) and paraventricular (PVH) hypothalamus, whereas it stimulates fatty acid oxidation in muscle by activating AMPK in this tissue. Here we found that a novel protein phosphatase, CIPP (CaMKK-AMPK cascade–inhibitory protein phosphatase), dephosphorylates and suppresses the activity of CaMKKβ in response to leptin, thereby inhibiting AMPK activity, in neuroblastoma cell line SH-SY5Y and in mouse ARH.
Methods
CIPP was found from the NCBI database and expression in SH-SY5Y cells and mouse ARH.
Results
CIPP belongs to the PP2C family and was expressed in human brain as well as SH-SY5Y cells and mouse ARH, but not in mouse or human skeletal muscle. CIPP was expressed in a part of NPY neurons in the ARH. CIPP dephosphorylated threonine residue of CaMKKβ, then suppressing its activity in vitro. CIPP siRNA suppressed leptin-induced inhibition of CaMKKβ and AMPK activity in SH-SY5Y cells. Leptin induced the phosphorylation of CIPP in a manner dependent on PI3-kinase and Akt as well as the recruitment of CaMKKβ to CIPP, thereby triggering the dephosphorylation of CaMKKβ and AMPK, in SH-SY5Y cells and mouse ARH.
Conclusion
Our results suggest that CIPP mediates inhibition of AMPK activity in the ARH by leptin via inhibition of CaMKKβ activity. Furthermore, the tissue distribution of CIPP may underlie the mechanism by which leptin reciprocally regulates AMPK activity in the ARH and skeletal muscle.
Conflict of Interest: none of the authors have a financial interest related to this work. Funding: This study was supported by the Ministry of Education, Culture, Sports, Science, and Technology of Japan
Obes Facts. 2009 May 14;2(Suppl 2):165.
Introduction
In previous studies we showed a clear effect of viscosity on satiation/ad libitum food intake (1). So far, the underlying mechanism responsible for differences in satiation responses between liquids and solids is not clear. In other previous studies we found indications that oral processing time (OPT) and bite size could play a role (2). Therefore, our objective was to determine the effect of bite size and OPT on ad libitum food intake.
Methods
22 healthy subjects participated in all 7 conditions of the study. Bite sizes were free or fixed to small bite sizes (approximately 5 gram) or large bite sizes (approximately 15 gram). OPT was free or fixed to 3 or 9 seconds. Subjects consumed chocolate custard with a peristaltic pump to control bite sizes. Sound signals indicated duration of OPT.
Results
Preliminary analyses show a significant effect of bite size (P<0.05). In the small bite size conditions, ad libitum intakes were 380±198 gram (3sec OPT) and 312±170 (9sec OPT). In the large bite size conditions, ad libitum intakes were much higher, 475±176 (3sec OPT) and 432±163 (9sec OPT) gram.
Conclusion
Larger bite sizes led to a significant higher food intake.
Conflict of Interest: No conflict of interest. Funding: Research related to this abstract was funded by the Top Institute Food and Nutrition.
References
- 1.Zijlstra N, Mars M, de Wijk RA, Westerterp-Plantenga MS, de Graaf C. The effect of viscosity on ad libitum food intake. Int J Obes (Lond) 2008;32:676–683. doi: 10.1038/sj.ijo.0803776. [DOI] [PubMed] [Google Scholar]
- 2.de Wijk RA, Zijlstra N, Mars M, de Graaf C, Prinz JF. The effects of food viscosity on bite size, bite effort and food intake. Physiology&Behavior. 2008;95:527–532. doi: 10.1016/j.physbeh.2008.07.026. [DOI] [PubMed] [Google Scholar]
Obes Facts. 2009 May 14;2(Suppl 2):165.
Introduction
Previous studies have reported acetate ingestion (delivered in vinegar) significantly increases satiety. However these studies failed to quantitatively assess effects on satiety and to account for the taste effects of vinegar on appetite. The present study therefore aims to address these methodological weaknesses.
Methods
Sixteen unrestrained eaters (three male, thirteen female) aged 22.2 [SD 3.0] years were recruited to this randomised single-blind crossover study. Participants attended three study sessions where they consumed a standard breakfast alongside an unpalatable (Unpal) or more palatable (Pal) drink containing 25g vinegar or a drink without added vinegar (PL). Effects on appetite were assessed subjectively using visual analogue scales (VAS) and assessed quantitatively by providing a pre-weighed ad libitum pasta meal 3h post-prandially. Capillary blood samples were regularly collected by fingerprick to monitor the post-prandial glycaemic response.
Results
Pal and Unpal vinegar treatment significantly reduced subjective appetite ratings for the desire to eat (p=0.036) and hunger (p=0.045) and increased fullness (p=0.000) and also nausea (p=0.001) (repeated measures ANOVA) when compared to PL. However no significant effects on quantitative measures of appetite were observed, with a mean intake of 530 [SD 163]g, 497 [SD 154]g and 485 [SD 238]g of the pasta meal following PL, Pal and Unpal respectively. Vinegar treatment was also found to significantly lower the glycaemic response (p=0.022, repeated measures ANOVA).
Conclusion
While significant effects on appetite ratings were observed, actual intake 3h post-prandially was not significantly reduced. This suggests vinegar influences appetite only transiently, possibly due to increased nausea.
Conflict of interest: None. Funding: Research relating to this abstract was funded by Premier Foods
Obes Facts. 2009 May 14;2(Suppl 2):166.
Introduction
Saturated fatty acids (SFA) are strongly correlated to the obesity genesis. However, the consequences of high SFA consumption on central mechanisms involved in the regulation of food intake remain unclear. The aim of the present study was to investigate the effect of chronic consumption of lard-enriched diet on the central anorexigenic effect of insulin in rats.
Methods
2-mo-old male Wistar rats were fed for 8 weeks with: chow diet (C group) or lard-enriched diet (B group). Food intake and body weight were measured weekly. At the end of treatment, an intracerebroventricular (icv) cannula was stereotaxically implanted and after a recovering period of 7 days, rats received an icv injection of 20mU of insulin or vehicle (saline) and food intake was measured for the following 24h. After the sacrifice, epididymal, retroperitoneal and mesenteric depots were removed and weighted.
Result
B group (n=8) presented an increase of weight gain (167%, p<0,0001) and caloric intake (61%, p<0,0001) when compared to C group (n=8) in the last week of treatment. B group also presented an increase of epididymal (91%, p<0,05), retroperitoneal (162%, p<0,01) and mesenteric (78%, p<0,01) depots when compared to C group. Insulin icv injection did not alter food intake of B group (n=4) but promoted a nonsignificant decrease of 18% in C group (n=4).
Conclusion
Preliminary results suggest that chronic consumption of lard-enriched diet promotes a higher weight gain and fat storage and might impair the central anorexigenic effect of insulin.
Funding: FAPESP - The State of São Paulo Research
Obes Facts. 2009 May 14;2(Suppl 2):166.
Introduction
Our previous studies suggest that signals from fat tissue potentially drive hyperphagia following caloric restriction in mice, because hyperphagia persists until fat has recovered. Both leptin and TNF-α are suppressed during restriction and may be candidates driving the hyperphagic response. We replaced the depleted leptin or TNF-α in restricted mice to determine whether the hyperphagic response could be blunted.
Methods
Mice were restricted to 60% of ad libitum for 25 days. Before the end of restriction, they were implanted with a mini osmotic pump releasing either leptin, TNF-α or saline as a control (n=9), at a delivery rate that returned the hormones to ad lib levels. They were then released onto ad lib. food supply. Body (BM), fat (FM) and fat free mass (FFM), food intake (FI) and circulating hormones were measured throughout.
Results
BM, FM, FFM and levels of leptin and TNF-α all significantly decreased during the restriction period. Both leptin and TNF-α administration caused a blunted hyperphagic response, compared to saline, although they did not completely prevent it. Over the 8 days of measurement the saline group ate approximately 6g more food than the leptin or TNF-α groups and BM gain was consequently around 1.7g greater.
Conclusion
This study indicated that both leptin and TNF-α are likely to be involved in the control of appetite and body mass regulation after dieting. These compounds may be targets to minimise weight regain as people come to the end of dietary restriction.
Conflict of Interest: None Disclosed. Funding: Research relating to this abstract was funded by SEERAD (Scottish Executive Environment and Rural Affairs Department)
Obes Facts. 2009 May 14;2(Suppl 2):166.
Introduction
The aim of this study was to assess the effects of L-Leu supplementation in lactating dams, particularly, to analyze whether leucine is able to influence energy homeostasis through signalling mechanisms in the brain and contributing to improve body composition during lactation.
Methods
Animals were fed ad libitum with standard diet during pregnancy and supplemented with 2% L-Leu from delivery onwards. The number of pups per litter was adjusted to ten within 24h after parturition. Food intake, body weight and composition were periodically recorded. At day 21 of lactation, dams were sacrificed and blood samples and hypothalamus were collected for metabolic determinations.
Results
Food intake and body weight evolution did not statistically differ between control and Leu-treated animals. However, Leu-treated animals shown higher increase in body weight (measured between 25 days before parturition and day 17th of lactation) that could be attributed to higher increase in lean body mass, while not differences were seen in fat mass content. Study of hypothalamic gene expression showed that orexigenic peptides (AGRP and NPY) decreased in Leu group, whereas anorexigenic peptide expression (CART and POMC) were not different between groups. Expression of hypothalamic receptors of insulin (INSR), ghrelin, melanocortin (MC4-R) and leptin (ObRb) did not change by the treatment.
Conclusion
Our results point to the fact that dietary supplementation of Leu may modulate body composition during lactation contributing to higher lean mass. This would be accomplished by changes in transcriptome expression of hypothalamic neuropeptides modulating neuroendocrine control of food intake and adiposity signals.
No Conflict of Interest. Funding: AGL2006-04887, NUGO (FP6-506360), CIBER de Fisiopatología de la Obesidad y Nutrición is an initiative from ISCIII.
Obes Facts. 2009 May 14;2(Suppl 2):166–167.
Pregnancy is a state of physiological hyperphagia and represents a good model to unravel the mechanisms involved in feeding regulation. The hyperphagia is the main responsible for the positive energy balance in gestation, necessary for maintaining maternal energy stores. The presence of high serum-leptin levels and hyperphagia during pregnancy reflects a state of hypothalamic leptin resistance. In order to evaluate the responsible mechanisms of this leptin resistance state, we studied the signalling systems induced by leptin in the hypothalamus. Sprague-Dawley-rats in 13 and 18days of gestation were treated with leptin-icv. In the hypothalamus we determined leptin-receptor levels (Ob-Rb and low-forms) by western blot and RT-PCR, phosphorylation levels for STAT3 and Akt, and SOCS3 levels by western blot, weight and nocturnal food-intake were also measured. In the first-middle-part of pregnancy-(G13) the hypothalamic levels of p-STAT3 after leptin treatment showed a decreased in spite of normal levels of Ob-Rb. An increase in the levels of SOCS3 could be responsible for the alteration in this pathway. Interestingly Akt phosphorylation levels after leptin treatment are conserved. All this could explain the inhibitor effect of leptin on the food-intake at this gestational age. In the last-middle-part of pregnancy-(G18), leptin could not induce phosphorilation of STAT3 and Akt. The SOCS3 levels are increased and Ob-Rb levels are decreased. At this gestational age the inhibitory effect of leptin on food intake and weight is blocked. All this indicates that the hypothalamic leptin resistance during pregnancy develops progressively, with an early rise of SOCS3 levels, a blockade of STAT3 pathway, and a later reduction of Ob-Rb levels and a blockade of other signalling pathways like PI3K-Akt.
Obes Facts. 2009 May 14;2(Suppl 2):167.
Introduction
The consumption of high-fat diets is considered a risk factor for obesity development. However, the fatty acid composition of the diet seems to influence the effects of high fat content. In the present study, we investigated the effect of soy or fish oil-enriched diets on c-Fos-immunoreactivity (c-Fos-IR) as a marker of neuronal activation in hypothalamic nuclei involved in the control of feeding.
Methods
Male Wistar rats ate rat chow or chow enriched with soy (Soy-diet) or fish (Fish-diet) oil from weaning until 3-mo-old. Hypothalami were processed for c-Fos immunohistochemistry in both fasted and acutely refed rats.
Results
After fasting, no significant diet effect occurred. However, the response to refeeding was significantly influenced by diet. Fish-diet rats had increased c-Fos-IR in hypothalamic nuclei expressing anorexigenic modulators, as arcuate (127%, P=0.005), ventromedial (81%, P=0.03), paraventricular (161%, P=0.003), and dorsomedial (177%, P=0.00002). In Soy-diet rats, c-Fos-IR increased only in LH (303%, P=0.0005) which is rich in orexigenic neurons.
Conclusion
The lower activation of anorexigenic neurons and higher activation of orexigenic neurons in Soy-diet refed rats may indicate propensity to obesity development.
Funding: CNPq and CAPES
Obes Facts. 2009 May 14;2(Suppl 2):167.
Introduction
Nucleus accumbens (NAcb) is involved in palatability-induced feeding behaviour. Studies show a role of the central nitric oxide (NO) system in food intake regulation. We assessed if food intake modify NO release in the NAcb shell and whether this event can be altered by the long-term intake of a hyperlipidic palatable (HLP) diet.
Methods
Two-months-old female Wistar rats were fed ad libitum either a balanced control (46g lipid/kg) or a HLP (232g lipid/kg), enriched with lard and sugar, diet for 2 months. Microdilaysis membrane was implanted aimed at the NAcb shell and 30-min. microdialysate samples were collected with or without access to the respective diet. Dialysates were analyzed for NO by chemioluminescence.
Results
HLP animals presented heavier fat pads (p<0.01 and more carcass lipid content than C rats (p<0.01). Food intake failed to acutely change NO levels in the NAcb microdialysates and the chronic consumption of the HLP diet did not modify this response. L-Arginine infusion by reversed dialysis enhanced NO levels recovered in microdialysates (p<0.01).
Conclusion
Central NO system is not likely to participate in the acute effect of a HLP diet intake, at least after chronic exposure to this diet. Whether other brain areas or a short-term exposition to HLP diet differently affect NO system ought to be investigated.
Funding: FAPESP, CNPq
Obes Facts. 2009 May 14;2(Suppl 2):167.
Introduction
Understanding the nutrient and chemical sensing mechanisms in the gastro-intestinal tract (GIT) which act to trigger gut hormone release and appetite after food intake is crucial to be able to devise effective methods to reduce obesity. Recently, the sweet taste receptor (T1r2+T1r3) has been found to be expressed in endocrine L-cells throughout the GIT. Application of sucralose (a non-calorific, non-metabolisable sweetener) to L-cells in vitro stimulates GLP-1 secretion, an effect that is inhibited with co-administration of lactisole, a T1r2+T1r3 inhibitor.
Objective
We conducted a randomised-controlled trial in eight healthy volunteers to investigate whether ingestion of sucralose could stimulate GLP-1 and PYY release in healthy volunteers.
Methods
The study was conducted with local Ethical Committee approval. Following a 12hr fast, subjects consumed 50ml of either water, sucralose (0.083%w/v) or a non-sweet, glucose-polymer matched for sweetness (50%maltodextrin + 0.083%sucralose). Appetite ratings and blood samples were taken for 2hr and caloric intake was measured at lunch. Plasma GLP-1, PYY, insulin and glucose were calculated as incremental area under the curve (iAUC).
Results
Sucralose ingestion had similar effects to water ingestion and did not increase plasma GLP-1 (−358.6±401.3 vs. −675.0±1609.9 respectively) or PYY (−56.08±192.3 vs. −179.3±119.4). Maltodextrin significantly increased insulin and glucose compared to water (p<0.001) and showed a non-significant trend towards increased PYY and GLP-1. Appetite ratings and food intake were similar for all groups.
Conclusion
At this dose the non-calorific, non-metabolisable sweetener Sucralose does not stimulate a detectable plasma GLP-1 or PYY rise and does not reduce appetite in healthy volunteers.
Obes Facts. 2009 May 14;2(Suppl 2):167–168.
Introduction
The aim of present study was to assess plasma concentrations of ghrelin and PYY in obese women with and without depression.
Methods
In 45 obese women without additional diseases (age 55.3±7.4 y) depression level was examined with the Beck's questionnaire. After evaluation the study group was differentiated into subgroups: A–no depression (4.4±2.6 points), B-mild depression (12.1±1.9 points), C-severe depression (22.0±5.2 points). Blood samples were taken in the morning after an overnight fast. Plasma concentrations of ghrelin and PYY were measured by ELISA.
Results
We did not observe differences of serum concentrations of ghrelin and PYY between subgroup A and subgroups B and C. No correlations between depression level and serum concentrations of ghrelin and PYY were found.
| A | B | C | |
|---|---|---|---|
| n | 12 | 10 | 23 |
| Age (years) | 54.1±5.1 | 56.0±7.6 | 55.6±8.5 |
| Body mass (kg) | 106.1±11.8 | 96.3±12.0 | 101.2±19.5 |
| BMI (kg/m2) | 39.6±3.7 | 36.2±4.2 | 39.3±6.8 |
| Waist circumference (cm) | 103.8±30.0 | 102.5±9.4 | 110.3±12.5 |
| Fat mass (kg) | 52.2±10.3 | 49.0±12.3 | S1.2±16.2 |
| Ghrelin (pg/ml) | 73.4±20.4 | 79.3±14.4 | 75.3±24.5 |
| PYY (pg/ml) | 33.5±12.6 | 27.5±10.6 | 25.7±12.5 |
Conclusion
It seems that plasma concentration of PYY and ghrelin did not exert influence on depression level in obese women.
Obes Facts. 2009 May 14;2(Suppl 2):168.
Introduction
Given the importance of dietary and nutritional factors in management of type 2 diabetes mellitus this study was designed and carried out to explore the effect of sesame oil on blood glucose and lipid profile of type 2 diabetic patients at Yazd Diabetese Research Center.
Methods
A quasi-experimental study, following approval by Iran University of Medical Sciences'Ethics Committee for Human Studies, was conducted on 25 patients with type 2 diabetes mellitus(age:51.50±6.28y; BMI:27.30±3.00Kg/m2; disease duration:7.08±5.03y; Fasting blood glucose level:181.00±51.90 mg/dl). Subjects received 30g/day sesame oil in place of other cooking oils for 42 days. Plasma glucose, glycated hemoglobin (HbA1c), lipid profile [Total cholesterol(TC), Low –density lipoprotein cholesterol (LDL-C), High-density lipoprotein cholesterol(HDL-C) and Triglycerides(TG)]were measured at baseline and after 42 days of sesame oil substitution. 24 hours recalls were obtained at the first, middle and end of study. Data were analyzed using analysis of variance with repeated measure and paired t-test.
Results
Following 42 days intake of sesame oil, there were significant decreases in FBS (181±51.93 vs 154±39.65 mg/dl),HbA1c(9.64±2.00 vs 8.40±1.74 percent), TC (226.68±31.40 vs 199.80±37.87 mg/dl),LDL-C(123.90±34.56 vs 95.53±32.54 mg/dl) compared to pre-treatment values(P<0.05). Blood TG level decreased after intake of sesame oil but this difference was not significant. Also the changes of HDL-C levels were not meaningful.
Conclusions
Sesame oil resulted in considerable decrease in blood sugar, HbA1c and blood lipids(TC and LDL-C) in type2 diabetics.
Funding: Research relating to this abstract was funded by a grant (P/402) awarded by Vice Chancellor Office for Research affairs of Iran University of Medical Sciences.
Obes Facts. 2009 May 14;2(Suppl 2):168.
Introduction
Dietary fat plays a critical role in the development of the metabolic syndrome (MetS). This study aimed to assess the differential acute and chronic effects of dietary fat quantity and quality on postprandial lipoprotein metabolism in MetS patients.
Methods
130 MetS patients were randomly assigned to one of four isoenergetic diets distinct in fat quantity and quality: high-SFA (HSFA); high-MUFA (HMUFA) and two low-fat, high complex carbohydrate (LFHCC) diets, supplemented with 1.24 g/day of long chain n-3 PUFA (LC n-3 PUFA) or placebo for 12 weeks each. Postprandial plasma and triglyceride (TG)-rich lipoprotein (TRL) metabolism was assessed pre-and post-intervention.
Results
Post-intervention subjects who consumed the HMUFA or LFHCC n-3 diet had significantly lower postprandial plasma TG (P<0.001) and large TRL-TG (P=0.009) concentrations compared to subjects adhering to the other two diets. The effect of dietary change on postprandial metabolism pre- versus post-intervention demonstrated that the LFHCC diet increased the area under the curve (AUC) for total plasma TG (P=0.043), large TRL TG (P=0.010), TRL-C (P<0.001) and TRL retinyl palmitate (RP) (P<0.001). In contrast, the LFHCC n-3 diet did no induce postprandial triglyceridemia and reduced postprandial plasma cholesterol (P=0.005), apoB (P=0.003) and plasma ApoA1 (P=0.039) AUC.
Conclusion
A HMUFA diet can lower postprandial lipoprotein abnormalities associated with the MetS compared with both high- or low-fat diets (HSFA and LFHCC). Also the adverse TG raising effects of the long-term LFHCC diets were avoided by concomitant LC n-3 PUFA supplementation to weight-stable MetS subjects.
Conflict of Interest: None of the authors has any conflict of interest that could affect the performance of the work or the interpretation of the data. Funding: This study was supported in part by research grants from the European comunity (LIPGENE European proyect-505944 to López-Mirada, Roche), Consejería de Salud, Junta de Andalucía (P06-CTS-01425 to López-Miranda), the Spanish Ministry of Health (CB06/03/0047 (CIBER Fisiopatología de la Obesidad y Nutrición is an initiative of ISCIII)).
Obes Facts. 2009 May 14;2(Suppl 2):168–169.
Introduction
Oxidative stress may play a important role in the pathogenesis and development of ischemic heart diseases and obesity as well. Reactive oxygen species might be removed or inactivated by diet-derived (exogenous) antioxidants. The aim of this study was to investigate whether a diet rich in red beetroot products would affect the antioxidant capacity of human plasma.
Methods
A randomized, study was executed in group of fifteen obese women, age 65y (+/-4y), suffered from ischemic heart disease (IHD). All subjects received during 6 weeks red beetroot juice or fat free beetroot crisps in determined daily portions. Nutritional status (body composition, skinfold thickness), and lipid profile were estimated before and after dietetic intervention as well as concentration in plasma Total Antioxidants Status (TAS). The nutritional value of the daily diet (antioxidants vitamins, saturated fatty acids supply), was controlled during the whole intervention period by 24h recall.
Results
The six weeks long administration of red beetroot products, caused a significant increase TAS about 11%. No changes in nutritional status parameters and nutritional density of diets (antioxidants vitamins, fat supply) were observed.
Conclusions
Daily intake selected beetroot products can significantly improve the plasma antioxidant capacity of obese, suffered from IHD women.
Obes Facts. 2009 May 14;2(Suppl 2):169.
Introduction
The melanocortin-4 receptor (MC4R) is part of an important pathway regulating energy balance. In a previous study, we have demonstrated that the generation of antibodies (Abs) against the N-terminal domain of the MC4R in rats induced a mild obese phenotype associated with insulin resistance. These findings prompted us to search for functional anti-MC4R autoAbs in sera of obese patients.
Methods
Auti-MC4R autoAbs were detected after screening sera from 216 patients with different body mass index (BMI) by using direct and inhibition ELISA with an N-terminal sequence of the MC4R. Binding to the native MC4R was evaluated by flow cytometry with HEK-293 cells expressing the human MC4R and pharmacological properties of the autoAbs were assessed by measuring adenylyl cyclase activity.
Results
Positive results in all tests were obtained in 5 patients with overweight or obesity (prevalence: 3.6%) but not in normal weight patients. The selective binding properties of the anti-MC4R autoAbs were confirmed by surface plasmon resonance and immunoprecipitation with the native MC4R. Moreover it was demonstrated that these autoAb acted as non-competitive antagonists in vitro. One of these autoAbs was evaluated in vivo and increased food intake in rats after passive transfer via intracerebroventricular injection.
Conclusion
The fact that functionally active autoAbs were only present in overweight and obese but not in normal weight subjects strongly suggests a possible pathogenic role. Such inhibitory anti-MC4R autoAbs might therefore contribute to the development of obesity in a small subpopulation of patients.
Conflict of interest: None disclosed. Funding: No funding
Obes Facts. 2009 May 14;2(Suppl 2):169.
Introduction
Tungstate has proved to be a novel antiobesity agent, acting on energy expenditure and body weight gain through leptin pathway, and modifying brain neuropeptide levels. Based on these results we investigated the molecular targets of tungstate on the CNS.
Methods
A hypothalamic cell line was cultured with or without leptin, tungstate, MAPK and JAK2 inhibitors (including overexpression of SOCS3). We analyzed gene and protein expression, and intracellular location of different leptin pathway proteins. We administrated tungstate to wistar rats by ICV at the 3V as an in vivo model. We performed proteomic analysis from isolated hypothalamic nucleus (ARC, LHA and PVN) using obese/control mice, treated or not with oral tungstate.
Results
In-vitro, tungstate treatment increases P-JAK2 (2,5 fold, p<0,05), but does not alter the P-Tyrosine-STAT3. Treatment also increases PERK (7,6 fold, p<0,001) and P-Serine-STAT3 (2,6 fold, p<0,01), favouring its accumulation in the nucleus (1,8 fold) to induce gene expression. Tungstate ICV administration entails a 27,6% food intake reduction and a 25,6% body weight gain reduction. Proteome analysis of hypothalamic nucleus showed different protein expression profile between lean/obese and W treated/non-treated animals.
Conclusions
We have identified ERK in the leptin pathway as the molecular tungstate target in neural cells. This increase in P-MAPK induces an increase in P-Serine-STAT3, modulating gene expression. Tungstate administration decreases food intake and body weight gain (ICV) and modifies hypothalamic protein expression profile. As a whole, these results demonstrate a direct central effect of tungstate modulating energy homeostasis.
Obes Facts. 2009 May 14;2(Suppl 2):169–170.
Introduction
Childhood obesity is associated with increased cardiometabolic risk. Several risk factors have been described, namely homocysteine plasma levels.
Methods
56 children (29 boys; 27 girls; BMI>95th percentile) between 7-9 year-old participated in a lifestyle intervention program. Assessment at baseline included weight, height, BMI, BMI-Zscore (BMI-Zs), waist circumference (WC), Tanner stage, blood pressure (systolic (SBP) and diastolic (DBP)) and fasting serum level of glucose, insulin, C-peptide, total cholesterol, HDL, LDL, triglycerides (TG), leptin, interleukin 6 (IL-6), homocysteine and folic acid. Insulin resistance (IR) was calculated by FGIR method. Results with statistical significance (p<0.05) are presented.
Results
At baseline, all children presented with abdominal obesity (WC≥90th percentile). IR (FGIR<6) was observed in 9% of children and 40% showed hypertension. Total cholesterol ≥180 mg/dl and TG≥100 mg/dl were found in 36% and 16%, respectively. Correlation analysis showed a linear relationship between BMI and the following variables: SBP, insulin, C-peptide, IR, leptin and TG. WC correlated positively with BMI, BMI-Zs, SBP, C-peptide, insulin, IR, leptin and homocysteine, and negatively with folic acid. IR correlated linearly with SBP, C-peptide, TG, leptin and homocysteine, and inversely with folic acid. The plasma levels of homocysteine showed a positive correlation with weight, insulin, C-peptide, leptin, IL-6 and TG. However, folic acid levels were inversely correlated with homocysteine, BMI, DBP, insulin, C-peptide, leptin and TG.
Conclusions
These obese children showed a significant prevalence of dyslipidemia, IR and hypertension, which were correlated with higher homocysteine levels. In contrast, folic acid seems to have a protective role.
Conflict of interest: None declared. Funding: No funding
Obes Facts. 2009 May 14;2(Suppl 2):170.
Introduction
Dietary carbohydrates have been shown to impact lipid metabolism and cardiovascular disease (CVD) risk. The objectives of this study were to compare the effects of high vs low glycaemic diets on plasma lipids and genes involved in hepatic lipid metabolism in rats with dietary-induced obesity (DIO).
Methods
Male Sprague-Dawley rats (n=45) with established DIO were divided into 4 groups and fed low glycaemic amylose (AMO) or high glycaemic amylopectin (AMN) starch diets in an ad libitum or energy-restricted (ER) paradigm for 4 weeks. At the end of the experiment, overnight-fasted rats were killed, and blood and liver were harvested for serum lipid and gene expression analyses.
Results
AMO led to lower serum concentrations of triglycerides, total and HDL-cholesterol than AMN, but only when rats were fed ad libitum (p<0.05). Semi-quantitative RT-PCR showed lower relative mRNA levels for 7α-hydroxylase in the liver of rats fed ad libitum vs ER-AMN (p<0.05). On the other hand, relative levels of the LDL-receptor mRNA were higher in ER vs ad libitum feeding, independent of the diet (p<0.01). The type of starch did not affect relative mRNA levels of HMG-CoA reductase or fatty acid synthase. Western blot analyses of hepatic lipoprotein receptors are in progress.
Conclusions
A low glycaemic diet improves lipid metabolism under free feeding conditions, but has no advantage over a high glycaemic diet when energy intake is restricted. Differences in relative mRNA levels of genes involved in hepatic lipid metabolism account only partly for the benefits of the low glycaemic diet.
Obes Facts. 2009 May 14;2(Suppl 2):170.
Background
An excess in protein intake could lead to obesity and surely overload the immature renal function of the infant. A formula with the protein ratio of 1,2g/100ml confirmed its efficacy and tolerance in a clinical trial(Turck et al. JPGN 2006, 43:364-371). Several studies have enlightened the positive role of the lactose on colic flora and absorption of micronutriments.
Objectives
To evaluate a new infant formula with a carbohydrate fraction of 100% lactose and 1,2g/100ml proteins.
Methods
On term new-borns (< 7 days) were randomized to receive until the end of the 4th month(M4) exclusively, the studied formula (Group L)with 7,5 g/100 ml lactose, or the former formula (Nidal Novaïa 1®, Group N) with 6,4g/100ml lactose and 1,1g/100ml maltodextrin. Both formulas are otherwise strictly identical. Formula L's non inferiority was evaluated with the average daily weight (ADW) variation by an ANCOVA analysis of the Per Protocol (PP) population. Tolerance was assessed as secondary criteria on the Intention To Treat population (ITT).
Results
Were included 184 newborns(ITT=178 infants; PP=137 infants). ADW was under the non inferiority range (+/-2.5g/d). The daily intake in ml/kg was significantly lower in the group L (ITT = −5.28ml/d/kg; p<0.007). Frequency of undesirable events including transit disorders were similar in the two groups.
Conclusions
These results validate the efficacy and tolerance of this formula and prove that a formula should be seen in its globality. Protein and carbohydrate changes of the formula leads each time to lower intake suggesting a better proteino-energetic use.
Obes Facts. 2009 May 14;2(Suppl 2):170.
Introduction
Polyunsaturated fatty acids (PUFAs) composition of neural membranes is a key factor for brain development and function including cognition.
Methods
In rat studies supplementation and moderate deficiency of PUFAs were maintained during fetal development and early postnatal age and their impact on fatty acid composition of different phospholipids and on behavioural development and cognition ability up to old age were followed. Four ages were compared: 12th postnatal day, puberty, adult (12-month) and old (28-month) ages. Fatty acids were determined by gas chromatography. Spatial learning behaviour in Morris water maze was tested in the adult and 28 months old ages and behavioural stress sensitivity was also investigated at the adult age.
Results
As a result of PUFA supplementation the content of n-3 docosahexaenoic acid (DHA) increased in most of the phospholipid fractions starting from the age of 12 days up to the one year old adult age. By the old age no difference in the fatty acid composition of nervous tissue membranes were detected any more between groups, however behavioural effect could be found even in the 28 months old age. The PUFA supplementation improved spatial learning, while the moderate PUFA deficiency acted into the opposite direction in cognition and decreased resistance against psychic stress.
Conclusion
Both the supplementation and the deficiency of PUFAs during development have long-term effect on fatty acid composition of nervous tissue membrane phospholipids up to adult age, but the functional consequences on cognition lasted even longer up to the old age of 28 months. Supported by Hungarian Scientific Research Fund (OTKA) K68875 and Ministry of Health Research Grant (ETT) 21/2006 to CN
Obes Facts. 2009 May 14;2(Suppl 2):170–171.
Introduction
The expression of total leptin receptor (Ob-R) and the long-signalling form (Ob-Rb) were measured by real time RT-PCR in PBMC to determine whether changes could be detected with obesity and ageing in humans.
Methods
Blood was sampled from lean (n= 8; BMI, 20-26 kg.m−2) and obese (n= 5; BMI 30-36 kg.m−2) young (23-38 years) men as well as lean (n= 9; BMI, 20-26 kg.m−2) and obese (n= 7; BMI 30-36 kg.m−2) older men (50-64 years). Reverse transcribed cDNA from PBMC cells was amplitied by PCR using primers to Ob-R and Ob-Rb on an ABI Prism 7700 under the following conditions; 50 C (2 min) for 1 cycle, 95 C (10 min) 1 cycle, 95 C (15sec), 60 C (1 min) for 40 cycles. Values were standardised to beta actin. The study was approved by the local ethics committee (NOSREC).
Results
Two-factor ANOVA on the log of leptin receptor expression in the PBMC revealed a correlation of Ob-R mRNA expression with age and obesity and an interaction between age and obesity for both Ob-R and Ob-Rb.
Young lean (Y-L), Young obese (Y-Ob), Older lean (O-L), Older obese (O-Ob)
| ANOVA | Age | Obesity | Age.Obesity |
|---|---|---|---|
| Ob-R | p<0.001 | p<0.001 | p<0.001 |
| Ob-Rb | p=0.021 | p=0.014 | p<0.001 |
Conclusion
This indicates that the expression of the leptin receptor in PBMC may be a potential biomarker of leptin insensitivity in obesity and ageing.
Funding: This work was funded by the European Union, project number QLK6–2002-02288 (OB-AGE) and by the Scottish Government, Rural and Environment Research and Analysis Directorate (RERAD).
Obes Facts. 2009 May 14;2(Suppl 2):171.
Purpose
To investigate the sex associated differences in energy metabolism, we evaluated some parameters of energy metabolism in both male and female rats when given high fat diet.
Methods
Three weeks old male and female SD rats were fed with standard chow for a week. We separated them into standard chow (C: fat 10%) and high-fat diet (HF: fat 60%), respectively, and kept them for a week. Then rats were sacrificed and mRNA expressions of leptin, NPY, AGRP, and POMC were examined by qRT-PCR. Serum glucose, insulin and leptin concentrations were measured by ELISA.
Results
We did not observe any significant difference in energy intake and body weight gain among 4 groups (male C, male HF, female C, and female HF). Male HF showed significantly high levels of serum leptin and insulin as compared to other groups. Leptin mRNA expression of male HF was also significantly high. Male HF showed a decrease in NPY and AGRP mRNA expressions, but female HF did not. On the other hand, POMC mRNA of female HF significantly increased.
Conclusion
We observed no significant differences in either energy intake or body weight gain among these 4 groups. However, male rats fed with HF for a week showed hyperinsulinemia and hyperleptinemia, indicating that there are significant differences in response for energy metabolism to HFD between male and female rats.
Obes Facts. 2009 May 14;2(Suppl 2):171.
Introduction
The bone mass attained during growth is a critical determinant of the risk of osteoporosis later in life. Despite the epidemic of childhood obesity, the effect of obesity on bone mineral accrual during growth is not well understood. The aim of this study was to analyze body composition and bone mineral content (BMC) and density (BMD) of the skeleton in obese prepubertal children.
Methods
We examined 45 obese patients at the age 5-10 years. Physical examination including height and weight was performed and body mass index (BMI) was calculated. Regional and total BMC, BMD and body composition were measured by dual-energy X-ray absorptiometry. We compared these results with those of 30 healthy non-obese children at the same age.
Results
The obese children had greater lean tissue mass (24.78±5.14 vs 20.09±3.96 kg; p<0.001), fat mass (19.00±6.68 vs 5.84±1.81 kg; p<0.0001), total BMC (1.28±0.36 vs 0.91±0.22 kg; p<0.0001) and BMD (0.89±0.07 vs 0.82±0.05 kg/cm2; p<0.001) than non-obese subjects. Lumbar spine (L1-L4) BMD was also greater in patients as compared to lean children (0.77±0.11 vs 0.66±0.08 g/cm2; p<0.0001). Body fat % and BMI showed positive correlation with BMC and BMD of spine and whole body measurements.
Conclusions
Our results indicated that obesity during prepubertal period may be associated with increased vertebral bone density and increased whole-body bone mass. Further studies are needed to determine bone mass after lifestyle intervention in these children.
Obes Facts. 2009 May 14;2(Suppl 2):171.
Introduction
Simple obesity and its adverse health effects need efficient dietary treatment and behavior therapy in children and adolescents. Anthropometric parameters may not identify all positive changes associated with lifestyle modifications. The aim of this study was to investigate if leptin and soluble leptin receptor can be clinically useful in prepubertal obese children before and after weight loss.
Methods
We determined changes in clinical, anthropometric and metabolic parameters, including leptin and leptin receptor in 26 patients at the age 4-10 years before and after the 3- months intervention program. Lifestyle intervention consisted of dietary and physical activity modifications and behavior therapy including individual psychological care of the child and his/her family. Serum leptin and leptin receptor concentrations were measured by ELISA kits from DRG (Germany).
Results
In obese children after the 3-months therapy we observed decreased concentration of leptin (about 50%; p<0.001) and increased concentration of leptin receptor (about 20%; p<0.05) in comparison to baseline. Negative significant correlation between both markers showed the normalization of these parameters after weight loss. We observed lower body mass index (BMI) (about 10%; p<0.05) in children with lifestyle intervention.
Conclusions
Our results suggest that leptin and leptin receptor may identify in obese children the positive changes that are associated with lifestyle modifications. However, further studies with long-term observation of presented patients are necessary to confirm the efficacy of these biochemical markers measurements in the management of prepubertal obese children.
Obes Facts. 2009 May 14;2(Suppl 2):172.
Introduction
This study examined the possibility that water-induced thermogenesis (WIT), a drinking of water could augment the increment of resting energy expenditure (REE) by using a precision indirect gas-analysis system in well-trained female volunteers. We also examined whether or not the thermogenic response was influenced by carbonate or mineral in the water.
Methods
This study was a randomized, crossover-design. Ten nonobese females (22.1±0.2 yrs) were given 250 ml (15°C) of soft-water or carbonated soft-water or hard-water (hardness:1468) or nothing (control) at random on four separate days. REE and autonomic nervous system (ANS) activity, assessed by heart rate variability, were measured for 15 min before drinking and 60 min after drinking. The 60-min WIT was calculated in two ways 1) as the delta increase above the pre-drinking REE and 2) as the delta increase above the value of control for the same period of time.
Results
In the control trial, REE gradually decreased with time. When regarded WIT of control as 0kJ, the values of WIT were follows; the hard-water was 23±6kJ (p<0.05, vs. control), the carbonated soft-water was 20±8kJ (p=0.087, vs. control), and soft-water was 15±8kJ (NS, vs. control), respectively. The activity of ANS seemed attributable for the increased thermogenic response, i.e. higher vagal activity was observed after drinking (p<0.05).
Conclusion
Strict condition of the test as well as improvement of gas-analysis system enabled to evaluate the delicate change in REE after water drinking. Our data suggest that the carbonate or mineral stimulate thermogenesis after drinking.
Conflict of Interest: Non Disclosed. Funding: Research relating to this abstract was funded in part by a Japanese Ministry of Education and Science Grant-in-Aid for Scientific Research (c) 18500626.
Obes Facts. 2009 May 14;2(Suppl 2):172.
Obesity increases breast cancer incidence rates in postmenopausal women. Chronic high levels of insulin, present in the majority of obese and insulin resistant patients, may provide the growth promoting stimulus to explain this connection. In this work, the cancer progression and cancer initiating properties of high insulin levels were examined in breast cancer cells (MDA-MB-231) and breast epithelial cells (MCF-10a), respectively.
High insulin levels (100 nM) induced differential changes in cell proliferation in the two cell lines used. Human Cancer PathwayFinder DNA Microarrays (SABiosciences) were used to examine gene expression changes after insulin treatment. High insulin levels increased expression of genes involved in cell cycle control (e.g. cyclin D1) and DNA damage repair (e.g. ATM) in MDA-MB 231 cells and in MCF-10a cells (e.g. cyclin E1, CDC25a). Expression of genes responsible for mediating apoptosis and cell senescence (e.g. APAF, BAD, bcl-X) was decreased after insulin treatment in MDA-MB 231 cells but the expression of the same group of genes did not change in MCF-10a cells. High insulin levels increased expression of genes encoding for signal transduction molecules (e.g. AKT1) and transcription factors (e.g. FOS, JUN, MYC), and of genes responsible for invasion and metastasis (e.g. MMP2) in MCF-10a cells whereas gene expression of the same groups of genes did not change or was decreased in MDA-MB 231 cells.
These results suggest a role for insulin resistance in breast cancer initiation and progression, aggravating the potential of breast cancer to evade apoptosis but to metastasise and may promote carcinogenesis of healthy epithelial cells.
Conflict of interest: None. Funding: Research relating to this abstract was supported by the Breast Cancer Campaign and the Research & Development Initiative, The Robert Gordon University.
Obes Facts. 2009 May 14;2(Suppl 2):172.
Introduction
Physical activity is important to prevent obesity-related co-morbidity. To become physically active on a regular basis, motivation is vital. The aim of this pilot study was to study motives for obese adolescents to becoming physically active, and to evaluate the effect on some risk factors for CVD during an intervention with personal coaching.
Methods
13 obese adolescents (14-17y) exercised with support from personal coaches during 10 weeks. After the exercise period, the adolescents filled out a questionnaire which dealt with their motivation. Fasting blood samples were drawn before and after the intervention.
Result
The group with high participation (>40%) was mainly motivated by intrinsic factors such as the joyful feeling connected to physical activity. The group with low participation (<40%) was mainly motivated by extrinsic factors. Social support was essential for the adolescents motivation to physical activity. No differences in inflammatory markers before and after the intervention were found, possibly due to few participants.
Conclusion
In an intervention aimed to increase physical activity among obese adolescents the coaching needs to focus both on intrinsic motivation and extrinsic motivational factors such as “social support”.
Conflict of interest: None Disclosed. Funding: Research relating to this abstract was funded by “Swedish Council of Working Life and Social Research” and “Swedish Research Council”.
Obes Facts. 2009 May 14;2(Suppl 2):172–173.
Introduction
Low adiponectin levels are associated with coronary artery disease and with type 2 diabetes. In the present study we examined the association between left ventricular arrhythmogeneity (LVA) with serum concentrations of adiponectin and with established risk factors for atherosclerosis in healthy subjects free of macrovascular disease and without metabolic syndrome according to the NCEP-ATP III criteria.
Methods
A total of 262 (113 male/149 female) healthy subjects (mean age 57±10.1 years) were included. % of body fat was determined using bioimpedance analysis. Fasting serum insulin and adiponectin levels were measured by RIA, while glucose and lipids by enzymatic methods. The homeostasis model assessment equation was used for the assessment of insulin resistance (HOMA-IR). LVA was assessed vectorcardiographically by determination of the spatial QRS-T angle (TCRT) on a 12-lead electrocardiogram using the MEANS program.
Results
Serum adiponectin levels were significantly and negatively associated with HOMA-IR and positively with HDL cholesterol. Univariate regression analysis showed that TCRT was associated significantly with adiponectin, gender, age, % of body fat, blood pressure, LDL cholesterol and high-sensitivity CRP. No significant association was found between the TCRT and HOMA-IR. Multivariate analysis, after adjustment for all associated factors, demonstrated that the TCRT was associated significantly and independently only with adiponectin, gender, LDL cholesterol and blood pressure.
Conclusion
In this apparently healthy population, no significant relationship was found between insulin resistance and LVA. On the contrary, low adiponectin levels were independent predictors of LVA. Therefore, our findings indicate that adiponectin may possess antiarrhythmogenic effects in humans.
Conflict of interest: none. Funding: None
Obes Facts. 2009 May 14;2(Suppl 2):173.
Introduction
Evaluation of metabolic disorders and prevalence of inflammation and oxidative stress in obese adolescents in Poland.
Methods
114 adolescents (10-18 yrs) with simple obesity formed study group, whereas 53 age matched lean subjects - control group. BMI, WHtR and WHR were calculated. Lipid profile was performed. Blood glucose and insulin were assessed during oral glucose tolerance test (OGTT). The presence of insulin resistance and metabolic syndrome (MetS) was determined. Inflammation factors (CRP, IL-6, TNF-α) and oxidative stress factors: transferin, uric acid, MDA, free thiols, advanced protein peroxidation products (AOPP) concentrations and antioxidant enzymes activities (Cu/Zn SOD, CAT, GPX) were determined.
Results
Overweight was diagnosed in 27 subjects (23,7%) and obesity - in 87 subjects (76,3%) (IOTF criteria). MetS was diagnosed in 43 subjects (43%). Type 2 diabetes was diagnosed in 2 patients (1,8%), impaired fasting glucose (IFG) - in 40 (35,4%), impaired glucose tolerance (IGT) - in 20 (17,7%). Number of clustering metabolic disorders, inflammation and oxidative stress increased along with the degree of obesity. Antioxidative defence was greater in obese and overweight children than in controls and lower in obese than overweight. Central obesity and MetS were associated with greater insulin resistance, dyslipidaemia, inflammation, oxidative stress. Antioxidative defense was decreased in central obesity but elevated in MetS.
Conclusions
The study indicates that both inflammation and the prooxidative-antioxidative imbalance are already present in childhood obesity. Oxidative stress and inflammation increase along with the degree of obesity, as well as with central obesity and with the clustering of metabolic disorders that form the MetS.
Obes Facts. 2009 May 14;2(Suppl 2):173.
Folic acid (FA) deficiency has been linked with an increased cardiovascular risk. FA is a key element for the proper functioning of the immune system. 87 pregnant women (30.44±4.33 years) were divided into two groups according to FA nutritional status (plasma): lower status, <12.5 nmol/L, (n=42), & higher status, ≥12.5 nmol/L, (n=45). Plasma lipid profile (LP), triglycerides (TG), total cholesterol (TC), cholesterol joined to high density (HDLc) and to low density lipoproteins (LDLc), leukocyte series and lymphocyte subpopulations (CD8+, CD4+, CD3 and CD16+56) were measured. The group of pregnant women with high status of FA showed higher levels of HDLc (mg/dL) (p=0004) (76.32±18.38 vs 87.29±16.72) and lower TG levels (185±61.76 vs 152.81±63.38; mg/dL). While total lymphocytes and its subpopulations were similar in both groups, neutrophils (10.88±2.85 vs 9.74±2.56; 103µL) were lower (p=0014 & p=0042, respectively) in the group with higher status of FA. Total leukocytes (103µL) were almost significantly lower in this group.
Conclusion
Adequate levels of FA throughout the gestational period appear to be associated with lower cardiovascular risk in the pregnant women. The results suggest a positive immunomodulator effect, confirming the importance of this vitamin during pregnancy.
Preliminary results of the PREOBE study, funded by Consejería de Innovación, Ciencia y Empresa de la Junta de Andalucía. (P06-CTS-02341). Spain.
Obes Facts. 2009 May 14;2(Suppl 2):173–174.
Introduction
The aim of the present study was to examine the associations of IL-6 with plasma lipids in lean and obese subjects.
Methods
We examined 115 women, 14 lean (age 41.4±8.0 y, BMI 23.1±2.7 kg/m2) and 101 obese (age 52.9±9.2 y, BMI 37.9±5.7 kg/m2). Anthropometric and biochemical parameters were measured. Blood samples were taken in the morning after an overnight fast. Plasma concentration of IL-6 was measured by ELISA and lipids by calorimetric methods.
Results
Obese subjects had higher level of IL-6. There were no differences in plasma concentrations of total and LDL-cholesterol between study groups. However, level of HDL- cholesterol was lower and triglycerides level was higher in the obese group than in lean subjects. In lean group IL-6 level was significantly related to plasma concentrations of total and LDL-cholesterol (r=0.70; p<0.05 and r=0.61; p<0.05 respectively). There were no correlations between IL-6 levels and plasma HDL-cholesterol and triglycerides in both study groups.
| Obese | Lean | p | |
|---|---|---|---|
| IL-6 (pg/ml) | 10.1±3.3 | 2.6±1.6 | < 0.0001 |
| Total–cholesterol (mg/dl) | 231.1±51.4 | 222.5±38.0 | NS |
| LDL–cholesterol (mg/dl) | 153.4±56.1 | 142.4±40.9 | NS |
| HDL–cholesterol (mg/dl) | 49.5±14.4 | 61.7±12.8 | < 0.0001 |
| Triglycerides (mg/dl) | 141.3±75.4 | 90.3±47.7 | < 0.0001 |
Conclusion
We conclude that IL-6 may be connected with cholesterol level in lean subjects, while in obese this effect may be suppressed by action of other adipokines.
Obes Facts. 2009 May 14;2(Suppl 2):174.
withdrawn
Obes Facts. 2009 May 14;2(Suppl 2):174.
Introduction
Gene expressions of the oxytocin- atrial natriuretic peptide (OT-ANP) system has been shown to be under estrogenic control in heart. The objective of present study was to investigate the effects of blocking the OT-ANP system, using an oxytocin antagonist (OTA), on the hepatic gene expression of ANP receptor, guanylyl cyclase-A (GC-A), and on inflammatory markers in ovariectomized (Ovx) rats.
Methods
Ovx and sham operated (Sham) rats were kept in a sedentary state for 8-wk. Ten days before sacrifice, Ovx and Sham rats were subdivided into OTA- (0.1 µg / g BW, ip, daily) and vehicle-treated groups. Gene expressions in liver were quantified by quantitative real-time polymerase chain reaction.
Results
Hepatic GC-A mRNA was significantly (P < 0.05) decreased in Sham and Ovx rats receiving OTA indicating the reduced action of OT-ANP system in liver. Hepatic C reactive protein (CRP) mRNA was decreased (P < 0.01) in Ovx rats compared to Sham rats. Administration of the OTA resulted in an increase in CRP mRNA in both Sham and Ovx rats (P < 0.01). In OTA-injected animals, NF-kB protein content was increased in Ovx compared to Sham rats (P < 0.01). Although Ovx caused an increase in liver and intra-abdominal fat accumulation, there was no effect of OTA on these parameters.
Conclusion
Our results suggest that the loss of ANP action in liver following OTA administration may represent a loss of protection of ANP on the development of inflammation in liver. This effect may be exacerbated with the withdrawal of estrogens.
Conflict of Interest: None. Funding: Research relating to this abstract was funded by the Canadian Institute of Health Research (JML; T 0602 145.02) and the Natural Sciences and Engineering Research Council of Canada (JML; 7594).
Obes Facts. 2009 May 14;2(Suppl 2):174.
Introduction
Epidemiological studies suggested serum gamma glutamyltransferase (GGT) within its normal range might be an early marker of oxidative stress. Oxidative stress and inflammation could play critical roles in the pathogenesis of vascular events. The aim of the study was to investigate association between GGT, C-reactive protein (CRP) and insulin sensitivity (HOMA) in severe obese hypertensive women and to compare these parameters with those obtained in severe obese normotensive women.
Methods
We investigated 13 obese hypertensive (HTA >/=140/90mmHg) women (age 36.38±2.41yrs; BMI 35.29±1.51kg/m2) and 13 normotensive obese women (age 33.61±2.09yrs; BMI 36.03±0.97kg/m2) with normal fasting glucose. CRP, GGT and HOMA index were determined in all women. Results: There was no difference (normotensive vs. hypertensive) in CRP (4.95±1.07 vs. 4.86±1.45mg/l, p>0.05), GGT (19.67±2.47 vs. 29.18±7.10mg/l, p>0.05), waist circumference (108.45±3.08 vs. 104.25±2.73cm, p>0.05) and in insulin sensitivity (HOMA) (4.54±0.84 vs. 3.48±0.59, p>0.05). There was positive significant correlation between CRP and BMI (r=0.734; waist (r=0.631) and HOMA (r=0.644) in normotensive women. There was no correlation between CRP and BMI, waist nether to HOMA index in hypertensive obese women. But there was significant correlation between CRP and GGT in hypertensive (r=0.877, p<0.001) and in normotensive obese women (r=0.836, p<0.05).
Conclusions
Our data confirmed significant correlation between GGT and CRP in obese women independent of value of blood presure and the level of insulin resistance. The strong association of serum GGT and CRP in obese women suggests their possible relationship and further studies are necessary to elucidate association between oxidative stress and inflammation in obesity.
Obes Facts. 2009 May 14;2(Suppl 2):174.
Introduction
The glycaemic properties of carbohydrates have been shown to affect determinants of energy balance and glucose metabolism. This study tested the hypothesis that a low-glycaemic starch improves body weight and glycaemic control in rats with dietary-induced obesity (DIO).
Methods
Male Sprague-Dawley rats (n=45) with established DIO and impaired glucose tolerance were divided into 4 groups and fed low glycaemic amylose (AMO) or high glycaemic amylopectin (AMN) starch diets in an ad libitum or energy-restricted (ER) paradigm for 4 weeks. At the end of the 3rd week, rats underwent an oral glucose tolerance test and serial blood samples were collected from the tail vein. At the end of the experiment, overnight-fasted rats were killed, and blood and tissues were harvested.
Results
AMO led to lower total energy intake, weight gain, fat pad mass, glycaemic response, and fasting insulin and leptin than AMN, but only when rats were fed ad lib (p<0.05). However, AMO-fed rats had higher total area under the curve for GLP-1 and PYY, independent of feeding paradigm (p<0.01). ER corrected most metabolic abnormalities observed in AMN rats fed ad libitum. Analyses of relevant gene expression patterns are in progress.
Conclusions
A low glycaemic diet improves weight and metabolic control under free feeding conditions, but has no advantage over a high glycaemic diet when energy intake is restricted. The effect of AMO on plasma GLP-1 and PYY can be attributed to its high resistant starch content, and does not necessarily reflect a property of all low glycaemic diets.
Obes Facts. 2009 May 14;2(Suppl 2):174–175.
Introduction
Our study compared the impact of hormonal changes (insulin, glucagon like peptide-1 (GLP-1), peptide YY (PYY)) on the improvement of satiety, between gastric bypass and gastric banding surgery, independently of weight loss.
Methods
One year prospective follow-up of two groups of obese and type 2 diabetic patients: 20 patients who had undergone gastric banding (GB group) and 30 patients who had undergone gastric bypass (BP group). Three evaluations were carried out: preoperative assessment, 10% weight loss and one year after surgery. Each evaluation consisted in collecting feelings of hunger and satiety by visual analogical scales and blood sampling in order to analyze insulin, total PYY and total GLP-1, fasting and then every 30 minutes during 6 hours following standardized mixed meal (387kcal).
Results
At 10% weight loss, area under curve (AUC) of hunger was lower (717±789 vs 1364±629, p=0.0123); those of satiety (2333±908 vs 1591±722, p=0.0126), GLP-1 (5526±2325 vs 2464±1193, p=0.0006) and PYY (51069±18717 vs 27832±2740, p= 0.0141) were higher in BP group than in GB group. At one year, weight loss was higher in BP group than in GB group (28±8% vs 13±7%, p<0.0001) and when adjusting for weight loss, only AUC of hunger remained lower (987±781 vs 1621±657, p=0.0062).
Conclusion
Gastric bypass early leads to increase post-prandial secretion of GLP-1 and PYY which improve satiety, better than gastric banding. The new findings are that these changes are initially independent of weight loss, but at one year only hunger remains lower, when adjusting for weight loss.
Conflict of Interest: None disclosed. Funding: Conseil Régional du Nord-Pas-De-Calais and European council (FEDEP).
Obes Facts. 2009 May 14;2(Suppl 2):175.
Introduction
Non-alcoholic fatty liver disease (NAFLD) is commonly associated with central obesity, insulin resistance, and type 2 diabetes. The main factor of NAFLD is obesity, but the main reasons of NAFLD in non-obese subjects are not clearly revealed. Therefore, this study was to evaluate the signifcance of body weight in early adulthood rather than current body weight and weight change in NAFLD.
Methods
We analyzed medical records of 83 non-obese adult patients with NAFLD. Also, 100 of non-obese subjects without NAFLD were analyzed with medical records as control group. The NAFLD diagnosis was determined by ultrasonography..
Results
1) The age of study subjects was 51.2±9.22 in NAFLD and 49.5±10.29 in control group. 2) There was a statistical difference of current body weight and peak body weight between NAFLD and control group (64.0±7.60 kg vs 61.5±8.82 kg P=0.042; 66.6±7.66 kg vs 62.5±8.89 kg, P=0.001, respectively). However, the difference of body weight in early adulthood between two groups was not significant (61.1±9.22 kg vs 60.6±8.33 kg).
3)The change in current body weight and peak body weight in their life compared to early adulthood was signifcantly greater in NAFLD than in control group (2.9±5.15kg vs 0.9±2.34 kg, P=0.001; 5.5±5.61kg vs 1.9±2.74 kg, P<0.001, respectively).
Conclusion
This study suggests that weight reduction could be considered for the treatment of NAFLD patients although current weight is not obese.
Obes Facts. 2009 May 14;2(Suppl 2):175.
Aim
Tracking the vector of insulin secretion and insulin sensitivity is a recognized means of studying glucose control over time. We investigated the impact of physical activity and BMI on glucose control loop behaviour in healthy children over a 3 year period.
Methods
Participants: 197 children (110 boys) from the EarlyBird cohort studied annually from 5-8y. Measures: BMIsds, glucose, insulin sensitivity (HOMA-%S), insulin secretion (HOMA-%B) and moderate and vigorous physical activity (MVPA, measured by accelerometer) averaged from four annual seven-day readings. Children were divided by median MVPA and BMIsds at 8y into four groups (thin- active, thin-inactive, fat-active, fat-inactive).
Results
HOMA-%S and HOMA-%B were indistinguishable between the four groups at 5y (p=0.98, 0.92 respectively). HOMA-%B then fell and glucose rose in all four groups, compensated for by rising HOMA-%S. However, in thin-active at 7y, fat-active at 7y and fat-inactive at 6y - but not in thin-active - the vector plot changed direction abruptly (to falling HOMA-%S, rising HOMA-%B) as insulin-sensitivity was saturated and compensation sought from remaining insulin-secretory reserve. Glucose rose in all groups 5-8y (4.3-4.7mmol/l, p<0.001). By 8y, HOMA-%S was highest in thin-active (355%), followed by thin-inactive (306%), fat-active (252%) and fat-inactive (207%) (p<0.001). HOMA-%B at 8y was highest in fat-inactive (78%), followed by fat-active (73%), thin-inactive (60%) and thin-active (53%) (p=0.001).
Conclusion
The inflexion at 6-7y was not apparent in thin-active children, and may represent early compromise of a control loop under pressure. Physical activity and BMI act independently, but physical activity seems the more important to glucose control.
Conflict of Interest: None declared. Funding: Research funded by Novo Nordisk UK Research Foundation, Bright Future Trust, Astra-Zeneca, GSK, CG Foundation, Diabetes Foundation, EarlyBird Diabetes Trust
Obes Facts. 2009 May 14;2(Suppl 2):175–176.
Introduction
This investigation was planned to assess the relative contribution of norepinephrine and epinephrine in the control of lipid mobilization during exercise in subcutaneous adipose tissue of men treated with octreotide, a somatostatin analog.
Methods
Eight lean and eight obese young men matched for age and physical fitness performed 60-min exercise bouts at 50% of their maximal oxygen consumption one day under placebo infusion and a second day under i.v. infusion of octreotide. Lipolysis and local blood flow changes in subcutaneous adipose tissue were evaluated using in situ microdialysis.
Results
Infusion of octreotide at rest and during exercise suppressed plasma insulin and growth hormone and enhanced lipid mobilization. Epinephrine release was fully blocked while exercise-induced norepinephrine increase was unchanged. Plasma atrial natriuretic peptide was higher during exercise under octreotide when compared to placebo in lean men only. Under placebo or octreotide infusion, no difference was found in exercise-induced increase in glycerol between the probe perfused with Ringer alone and with phentolamine (alpha-adrenergic receptor antagonist) in lean while an enhanced increase in glycerol was observed in the obese. Under placebo, propranolol (beta-adrenergic receptor antagonist) infusion in the probe containing phentolamine reduced by about 45% exercise-induced glycerol release; this effect was suppressed under octreotide infusion while norepinephrine was still elevated.
Conclusion
Performing exercise under octreotide which blocks, insulin, GH and epinephrine reveals a lack of norepinephrine involvement and the main role of epinephrine in the adrenergic regulation of exercise-induced lipid mobilization in subcutaneous adipose tissue in men.
Conflict of interest: none disclosed. Funding: Project sustained by the French Fondation pour la Recherche Medicale (FRM)
Obes Facts. 2009 May 14;2(Suppl 2):176.
Introduction
During stress, individuals may gain or loose weight, mainly when they have access to “comfort foods”, rich in carbohydrates and fat, that may also reduce stress-induced anxiety. We investigated if the access to comfort foods may alter the food intake and behavioral parameters in rats submitted to stress.
Methods
Adult male Wistar rats were assigned to groups: control (CO) and stressed rats (IS: footshock, 1 mA, 1 s, 15-25 s intervals; 30 min, 3 days) fed with commercial diet; or CO and IS rats allowed to choose between commercial diet and palatable diet. Two hours after the last IS session, rats behavior was evaluated in elevated plus maze (EPM) and open-field. Differences were considered significant when p<0.05 (ANOVA plus Newman-Keuls test).
Results
Rats preferred palatable (CO 46.8±1.3; IS 49.3±4.1 g/day) rather than commercial diet (CO 1.37±0.37; IS 1.37±0.59 g/day), with no difference between groups. IS rats decreased daily intake of commercial diet (CO 51.8±1,7; IS 45.9±1,3 g), but not palatable diet (CO 46.8±1.3; IS 49.3±4.1 g). IS decreased number of stretch attend postures (CO 9.10±1.17; IS 5.40±1.09) in EPM but no other analyzed parameters were altered. Access to palatable diet did not modify the number of entries and time spent on EPM open arms; number of crossing, hearing and grooming in the open-field.
Conclusion
Stress-induced reduction on food intake is inhibited when rats have access to palatable diet. The preference for this kind of food was not due to altered exploratory or anxiety-like behaviors. Moreover, stressed rats decreased risk assessment behavior.
Conflict of Interest: none disclosed. Funding: Coordenadoria de Aperfeiçoamento de Pessoal de Ensino Superior (CAPES)
Obes Facts. 2009 May 14;2(Suppl 2):176.
Introduction
The effect of stress on food intake is controversial. The β3 adrenergic agonist BRL 37,344, administered in the third ventricle or peripherally, produces a dose-dependent reduction on food intake. We investigated the effect of BRL37,344 on the feeding behavior, locomotor activity and anxiety-like behavior of rats submitted to stress.
Methods
Adult male Wistar rats were submitted to one daily 30 min duration session of unsignaled, inescapable footshocks (1 mA, 1 s, random 15-25 s intervals between shocks) in 3 consecutive days. Food intake was measured in rats that have free access to chow. Another group of rats was overnight fasted before the last stress session; after that received BRL37,344 (30 nM/Kg, ip) or saline; following, rats were allowed access to chow and the food intake was measured after 2 h. Then, rats were evaluated in the open-field. Data were analyzed by ANOVA plus Newman-Keuls test and were considered significant different when p<0.05.
Results
Stress decreased daily food intake (35.5±5.3; 24.1±2.9 g, n=9) in rats with free access to chow, but increased it during the re-feeding period (3.55±0.50; 4.68±0.19g); increased crossing (42.9±9.1; 64.6±5.7) and hearing (22.9±4.2; 41.9±4.9). BRL 37,344 decreased feeding behavior in control (saline 3.55±0.50; BRL 2.44±0.17 g) and in stressed rats (saline 4.68±0.91; BRL 1.77±0.07 g); increased crossing (stress BRL 71.77±7.95) and number of grooming (control BRL 0.66±0.23; stress BRL 2.60±0.52). Glucose, leptin and insulin plasma levels are being determined.
Conclusion
footshock stress and BRL 37,344 reduced food intake due to another factor than locomotor impairment.
Conflict of Interest: none disclosed. Funding: Coordenadoria de Aperfeiçoamento de Pessoal de Ensino Superior (CAPES) and Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
Obes Facts. 2009 May 14;2(Suppl 2):176.
Introduction
The literature reported that the stresses of life in modern society may contribute to the increased incidence of obesity in humans. Also, it has been demonstrated that stress could induce insulin resistance. Since, it has been demonstrated that when fish oil, rich in n–3 PUFA, is substituted for one third into the lipid fraction of the diet, insulin resistance could be prevented. The aim of this study was to evaluate the effect of fish oil diet on glucose tolerance test response in rats submitted to a foot shock stress.
Methods
30-day-old Wistar male rats were treated, during 8 weeks, with: control diet (C) containing 5% of soybean oil, or fish diet (F) containing 5% of fish oil. The animals were submitted (CS and FS) or not (CN and FN) to a foot shock stress sessions during 3 days. After this, oral glucose tolerance test (OGTT) was performed.
Results
No difference of body weight was observed among groups during all the experimental period. Basal glucose concentration was higher in CS and FS than CN. Similar glucose concentration during OGTT was observed among CN, FN and FS. However, high glucose concentration was observed in CS in relation to CN at 15 minutes after oral glucose load.
Conclusion
These results demonstrated that foot shock altered basal glucose concentration, independent of the diet treatment. However, fish oil diet treatment could prevent the glucose intolerance promoted by foot shock stress. These results could suggest that fish oil prevents insulin resistance promoted by stress.
Conflict of interest: None disclosed. Funding: Research relating to this abstract was funded by FAPESP and CAPES