Abstract
Aim
The aim of this study was to evaluate the effect of an aerobic exercise on serum level of liver enzymes and liver echogenicity in patients with non alcoholic fatty liver disease.
Background
Non alcoholic fatty liver disease (NAFLD) has different prevalence in various parts of the world. Obesity and low physical activity are main risk factors for the development of NAFLD.
Patients and methods
Ninety patients diagnosed by ultrasound as NAFLD was evaluated in a clinical trial as case (A) and control groups (B). The effect of aerobic exercise on changing in liver enzymes and liver echogenicity was assessed in cases compared with control group which were only on medical therapy.
Results
The mean age in the sample group was 37.6±8.3 in the 17-56 yrs age range. In group A, fatty liver was in stage I in 26 (57.8%) cases, stage II in 17 (37.8%), and stage III in 2 (4.4%). In group B, fatty liver was in stage I in 30 (66.7%) patients, in stage II in 14 (31.1%) and stage III in 1 (2.2%). After an aerobic exercise, serum level of liver enzymes and liver echogenicity in patients with non alcoholic fatty liver disease was significant improved in case group (ALT (P= 0.0001), AST (P = 0.01).
Conclusion
Considering the present study, we can suggest that a controlled aerobic exercise schedule can be helpful in the association of medical therapy in the treatment of NAFLD.
Keywords: Liver enzyme, NAFLD, Aerobic exercise
Introduction
Non alcoholic fatty liver disease (NAFLD) is a liver disorder that is accompanied with accumulation of triglisiride in hepatocyte. Pathologic changes in non alcoholic fatty liver disease are similar to alcoholic fatty liver disease but there is not any alcohol consumption or less than limit that can be damage to hepatocyte. These changes are in a spectrum from simple steatosis to steato hepataitis and finally fibrosis and then scirrhosis (1–5).
NAFLD has different prevalence in various parts of the world, though 20-30% prevalence has been reported in epidemiologic studies in western countries (2, 6–8). This disease can be seen in all ages but often middle aged people are affected (8). Now there are multiple methods for the diagnosis of NAFLD in the world. Sonography is one of these methods that are applied to the diagnosis of this disease with ruling out of other probable disease (9).
NAFLD is related to metabolic syndrome such as obesity, diabetes mellitus and hyperlipidemia. Since obesity and low physical activity are main risk factors for the development of NAFLD, life style modification considering weight loss and physical activity is thought to be as important alternative for treatment of this disease (10). A few studies performed regarding the quantity of the physical activity in NAFLD. But the advantages of physical activity has been shown very clearly (11). With considering of this reality surveying on specific affects of physical activity on non alcoholic fatty liver disease in the site of research is necessary. Therefore, the aim of present study was to evaluate the effect of an aerobic exercise on serum level of liver enzymes and liver echogenicity in patients with non alcoholic fatty liver disease.
Patients and Methods
In this non randomized clinical trial including 90 patients with established NAFLD divided equally in to case and control groups. The duration of this study was 12 months from December 2011 and December 2012. For the diagnosis of this disease, sonography with acceptable sensitivity and specificity was applied. Before the entering a patient to the study the height and weight of patient with minimal cloths was measured in both groups. For the measuring of height and weight SECA balance device has been used with the accuracy of 0.5 cm and 0.1 kg. Body Mass Index (BMI) was calculated with the using of weight/height2 in the start of the study in both groups. Also body composition of any patient in each group was determined in the start and the end of the study with the device of ZEUS9 bioelectrical impedance analysis. At the beginning of the study the measuring of liver enzymes (AST, ALT, ALP) and FBS and lipid profile (TG, Total cholesterol, HDL cholesterol) with enzymatic methods was measured. The level of LDL cholesterol was calculated with the formula of Fredwald, but if the level of TG was upper than 400 mg/dl, enzymatic methods was applied for the measuring of LDL cholesterol. On the other hands in control group medical therapy with 1000 mg vitamin C and 400 units vitamin E was prescribed. In case group in addition to the medical therapy similar to control group, thirty minutes aerobic exercise with maximal heart rate three times a week with the duration of three months was performed. At the end of the study, variation of the variables (mentioned above) in cases was compared with control group.
Patients with alcohol consumption more than 20cc per day, drug usage, viral hepatotropic positive or Wilson's disease, autoimmune disease, cholestatic disorders, renal, cardiovascular or thyroid disease, and patents with history of gastric bypass surgery, paraentral nutrition or cachexicia were excluded from this study.
Statistical analysis
The results of the study represented as mean ± standard deviation (SD), percentage and abundance using SPSS software version 16. For the comparison of quantitative variables Student T test and for the comparison of qualitative variables Chi Square has been applied and in the cases in which predictive value was less than 0.05, this result recognized significant.
Results
Totally 57 subjects (63/3%) were male and 33 subjects (36.7%) were female. In group A (case group) 29 (64/4%) were male and 16 (35/6%) were female and in group B (control group) 28 individuals (62/2%) and 17 persons (37/8%) were male and female respectively. The mean age of whole patients was 37.6±8.3 ranged between 17-56 years old. The mean age in cases and control was 35.6±9.2 (17-54) and 39.5±6.9 (26-56) years old respectively. The statistical analysis showed a significant difference regarding mean age in two groups (P = 0.02). Basic data in studied groups are presented in Table 1. Table 1 showed no statistically difference in cases compare to controls. Also Table 2 showed that the mean of biochemical test in cases before and after an aerobic exercise only for ALT and AST was significant.
Table 1.
Basic data in case and control groups
| Case (n = 45) | Control (n = 45) | P-value | |
|---|---|---|---|
| Height | 169.7±11.8*
(120–188) |
168.3±9.9 (147–189) |
0.56 |
| Weight | 84.2±1.3 (50–115) |
83.9±1.3 (59–120) |
0.91 |
| BMI† | 28.9±3.2 (22.4–36.8) |
29.5±4.1 (23–46.6) |
0.47 |
| DBP‡ | 72.8±8.1 (60–90) |
76.2±9.8 (60–100) |
0.08 |
Mean± standard deviation (range)
Body mass index
Diastolic blood pressure
Table 2.
The result of biochemical test in cases before and after an aerobic exercise
| Variables* | Before | After | P Value |
|---|---|---|---|
| FBS | 95.2±19.6 (62–193) |
95.2±16 (66–160) |
P = 0.98 |
| TG | 218.2±12 (82–687) |
188.6±8.6 (36–398) |
P = 0.18 |
| Total Chol | 190.6±35.5 (124–294) |
194.9±38.8 (90–284) |
P = 0.58 |
| LDL | 108.1±31.3 (49–184) |
112.2±36.1 (38–197) |
P = 0.57 |
| HDL | 42.4±9.7 (27–71) |
45.3±8.8 (29–71) |
P = 0.14 |
| AST | 41.5±2.7 (13–137) |
29±9.5 (15–53) |
P = 0.006 |
| ALT | 61.1±3.6 (14–185) |
44.9±2.4 (13–119) |
P = 0.01 |
| Alk.P | 165.9±61.4 (29–338) |
185±56.2 (45–400) |
P = 0.12 |
Mean±SD; FBS: fasten blood sugar; TG: triglyceride; Chol: cholesterol; AST: Aspartate aminotransferase; ALT: Alanine aminotransferase; ALP: Alkaline phosphatase
After the completion of aerobic exercise duration in both groups, serum level of liver enzymes and liver echogenicity in patients with non alcoholic fatty liver disease was decrease.
The degree of fatty liver in group A showed fatty stage 1 in 35 patients (77.8%), stage 2 in 4 patients(8.9%) and 6 patients(13.3%) without sonographic fatty liver. In group B fatty liver degree of 33 patients (73.3%) was in stage 1, 9 patients (20%) in stage 2 and fatty liver of 3 patients (6.7%) had been resolved by sonography. The difference in both groups was not statistically significant (P = 0.23).
Weight, BMI FBS, TG, HDL, AST, ALT and VFM, kg was statistically significant by comparison of basic information description before and after trial in group A (P < 0.05) (Table 3). This result was statistically significant in control group for weight, BMI, SBP, DBP, TG and LBM (P < 0.05) (Table 4).
Table 3.
The comparison of basic information description before and after trial in group A
| Variable* | Pre Trial | Post Trial | P Value |
|---|---|---|---|
| Weight | 84.2±1.3 | 82.1±11.9 | 0.0001 |
| BMI | 28.9±3.2 | 28±2.8 | 0.0001 |
| SBP | 112.7±14.9 | 110.2±11.7 | 0.06 |
| DBP | 72.8±8.1 | 71.9±14.4 | 0.35 |
| FBS | 95.2±19.6 | 90.6±14.4 | 0.01 |
| TG | 218.2±12 | 176±5.2 | 0.002 |
| Total Chol | 190.6±35.5 | 183.2±25.6 | 0.09 |
| LDL | 108.1±31.3 | 100±26.2 | 0.06 |
| HDL | 42.4±9.7 | 46.5±8.1 | 0.0001 |
| AST | 41.5±2.7 | 34.3±15.1 | 0.01 |
| ALT | 61.1±3.6 | 43.5±2.4 | 0.0001 |
| Alk.P | 165.9±61.4 | 157.9±54.2 | 0.12 |
| VFM, kg | 3.8±1 | 3.7±1.1 | 0.0001 |
Mean± standard deviation FBS: fasten blood sugar; TG: triglyceride; Chol: cholesterol; AST: Aspartate aminotransferase; ALT: Alanine aminotransferase; ALP: Alkaline phosphatase
Table 4.
The comparison of basic information description before and after trial in group B
| Variable* | Pre Trial | Post Trial | P Value |
|---|---|---|---|
| Weight | 83.9±1.3 | 83.3±12.9 | 0.02 |
| BMI | 29.5±4.1 | 29.4±4.1 | 0.04 |
| SBP | 127.2±18.3 | 123.4±17.7 | 0.0001 |
| DBP | 76.2±9.8 | 72.8±10.8 | 0.006 |
| FBS | 95.2±16 | 94.3±13.4 | 0.2 |
| TG | 188.6±8.6 | 172.4±7.6 | 0.04 |
| Total Chol | 194.9±38.8 | 193.8±34.3 | 0.6 |
| LDL | 112.2±36.1 | 115.8±26.9 | 0.6 |
| HDL | 45.3±8.8 | 46±8.4 | 0.5 |
| AST | 29±9.5 | 28±9.9 | 0.2 |
| ALT | 44.9±2.4 | 39.9±2.2 | 0.07 |
| Alk.P | 185±56.2 | 193.2±46.8 | 0.2 |
| VFM, kg | 3.5±1.5 | 3.3±1.5 | 0.7 |
| WHR | 0.9±0.1 | 0.9±0.07 | 0.2 |
| Body Fat, kg | 23.2±6.1 | 22.9±6.8 | 0.6 |
| LBM | 55±9.9 | 54.9±8.9 | 0.005 |
Mean±SD; FBS: fasten blood sugar; TG: triglyceride; Chol: cholesterol; AST: Aspartate aminotransferase; ALT: Alanine aminotransferase; ALP: Alkaline phosphatase
Discussion
As our results showed that NAFLD's pathologic changes are similar to pathologic changes that are seen in alcoholic fatty liver disease but there is not alcohol usage in NAFLD (1). NAFLD's prevalence is different in the worldwide, though 20-30% prevalence has been reported in epidemiologic studies in western countries (2). This disease can be seen in all ages but often middle aged people are more affected (8).
Sotodeh et al. in 2006 studied the effect of aerobic exercise in patients with non alcoholic fatty liver disease. The finding of this study followed this kind of exercise and showed the decrease of liver enzymes level (12). In this study we showed the statistical significant decrease of AST, ALT and ALP level in NAFLD patients after an aerobic exercise. In addition to liver enzymes decrease in our study, the decrease of lipid profile in cases was statistically significant.
In another study by Chen et al. in 2008, 23 patients with established NAFLD did intense cycling in duration of 2 hours a week for 10 weeks and they show that in the end of study the significant decrease in topography index, insulin resistance and sonographic finding (13). Also in our study body composition components such as body fat mass, visceral fat mass and body mass index and waist to hip ratio had statistical meaningful decrease but we couldn't show the statistically significant decrease in sonographically fat component in our patients. In a cross sectional study by Perseghin et al., the relation between physical activity and the component of liver's fat was reverse (14).
In a meta-analytic survey in 2008, physical activity (aerobic or inaerobic) in 375 patients with NAFLD had protective effect such as decrease in lipid profile and body composition (15).
In conclusion with respect of result of this study and comparison with the studies which is mentioned above we could conclude that in addition to medical therapy, controlled exercise trial can be helpful in the cure of non alcoholic fatty liver disease.
(Please cite as: Khaoshbaten M, Gholami N, Sokhtehzari S, Monazami AH, Rostami Nejad M. The effect of an aerobic exercise on serum level of liver enzymes and liver echogenicity in patients with non alcoholic fatty liver disease. Gastroenterol Hepatol Bed Bench 2013;6(Suppl.1):S99-S103).
References
- 1.Bisceglie AM, Mahachai V, Graham AS. Advances in the understanding and treatment on nonalcoholic fatty liver disease. Drugs. 2003;63:2379–94. doi: 10.2165/00003495-200363220-00001. [DOI] [PubMed] [Google Scholar]
- 2.Ruhl CE, Everhart JE. Epidemiology of Nonalcoholic fatty liver. Clin Liver Dis. 2004;8:501–19. doi: 10.1016/j.cld.2004.04.008. [DOI] [PubMed] [Google Scholar]
- 3.Angulo P. Nonalcoholic Fatty Liver Disease. New England J Med. 2002;16:1221–31. doi: 10.1056/NEJMra011775. [DOI] [PubMed] [Google Scholar]
- 4.Moller DE, Berger JP, Hui JM. Hepatic steatosis and insulin resistance. Pharmacol Ther. 2005;22:64–70. doi: 10.1111/j.1365-2036.2005.02600.x. [DOI] [PubMed] [Google Scholar]
- 5.Das SK, Mukherjee S, Vasudevan DM. Non-alcoholic Fatty liver disease: an under- recognized cause with emerging importance. Curr Sci. 2006;90:5. [Google Scholar]
- 6.Harrison SA, Kadakia S, Schenker S. Non-alcohololic steatohepatitis: what we know in the New Millennium. Am J Gastroenterol. 2002;97:2714–24. doi: 10.1111/j.1572-0241.2002.07069.x. [DOI] [PubMed] [Google Scholar]
- 7.Targher G, Zenari L, Bertolini L. Relation of nonalcoholic hepatic steatosis to early carotid atherosclerosis in healthy men. Diabetes Care. 2004;27:2498–500. doi: 10.2337/diacare.27.10.2498. [DOI] [PubMed] [Google Scholar]
- 8.Neuschwander BA, Caldwell SH. Nonalcoholic steatohepatitis: summary of an AASLD single topic conference. Hepatology. 2003;37:1202–19. doi: 10.1053/jhep.2003.50193. [DOI] [PubMed] [Google Scholar]
- 9.Matteoni CA, Younossi ZM, Gramlich T. Nonalcoholic fatty liver disease: a spectrum of clinical and pathological severity. Gastroenterology. 1999;116:1413–19. doi: 10.1016/s0016-5085(99)70506-8. [DOI] [PubMed] [Google Scholar]
- 10.Manco M, Bedogni G, Monti L, Morino G, Natali G, Nobili V. Intima-media thickness and liver histology in obese children and adolescents with non-alcoholic fatty liver disease. Atherosclerosis. 2010;209:463–68. doi: 10.1016/j.atherosclerosis.2009.10.014. [DOI] [PubMed] [Google Scholar]
- 11.Brunt EM. Nonalcoholic steatohepatitis: definition and pathology. Semin Liver Dis. 2001;21:3–16. doi: 10.1055/s-2001-12925. [DOI] [PubMed] [Google Scholar]
- 12.Sotodeh M, Tavangar M, Khadem F. Correlation of the serum levels of the ALT and AST with the degree of inflammation and fibrosis in the liver of patients with non-alcoholic steohapatitis: validation of the revisions applied on the Brunt scoring system. Hakim. 2006;8:1–8. [In Persian] [Google Scholar]
- 13.Chen SM, Liu CY, Huang HT. Effects of therapeutic lifestyle program on ultrasound-diagnosed nonalcoholic fatty liver disease. J Clin Med Assoc. 2008;71:551–58. doi: 10.1016/S1726-4901(08)70168-0. [DOI] [PubMed] [Google Scholar]
- 14.Perseghin G, Cobelli F, Espositto A. Habitual Physical activity is associated with intrahepatic fat content in humans. Diabetes Care. 2007;30:683–88. doi: 10.2337/dc06-2032. [DOI] [PubMed] [Google Scholar]
- 15.Sagi S, Goldsmith R, Webb M. Role of lisure time physical activity in nonalcoholic fatty liver disease: A population based study. Hepatology. 2008;48:1791–98. doi: 10.1002/hep.22525. [DOI] [PubMed] [Google Scholar]