Abstract
This study aimed to detect the association of the suppressor of cytokine signaling 3 gene (SOCS3) A+930-->G (rs4969168) single nucleotide polymorphism (SNP) and environmental factors with serum lipid levels in the Han and Mulao populations. Genotyping of the SOCS3 A+930-->G (rs4969168) SNP was performed in 752 of Han and 690 of Mulao participants using polymerase chain reaction and restriction fragment length polymorphism. The genotype and allele frequencies were significantly different between the Han and Mulao populations (GG, 57.71% vs. 51.16%, GA, 36.97% vs. 41.16%, AA, 5.32% vs. 7.68%, P = 0.023; G, 76.20% vs. 71.74%, A, 23.80% vs. 28.26%; P = 0.006; respectively). Serum apolipoprotein (Apo) A1 levels in Han were different among the genotypes (P < 0.05). Subgroup analyses showed that the levels of ApoA1 in Han females, and ApoA1 and low-density lipoprotein cholesterol (LDL-C) in Mulao males were different among the genotypes (P < 0.05). Serum lipid parameters were also associated with several environmental factors in both ethnic groups (P < 0.05-0.001). These findings suggest that there may be a racial/ethnic- and/or sex-specific association between the SOCS3 A+930-->G (rs4969168) SNP and serum lipid parameters in some populations.
Keywords: Lipids, suppressors of cytokine signaling 3, single nucleotide polymorphism, environmental factors
Introduction
Cardiovascular disease (CVD) is a major public health problem worldwide and affects individuals across all age groups and ethnicities [1]. World Health Organization (WHO) estimates that more than 17.3 million people died of CVD such as heart attack or stroke in 2008. Contrary to popular belief, four out of five of these deaths occurred in low-and middle-income countries, and men and women were equally affected (www.who.int). Dyslipidemia is a leading risk factor for CVD. However, due to various reasons, including considerable heterogeneity of dyslipidemia, the identification of susceptibility genes is difficult and most associations have not been replicated.
A multitude of genes associated with serum lipid levels have been discovered, with one of the most important being the suppressor of cytokine signaling 3 gene (SOCS3), which is located in the chromosome region 17q24-17q25. SOCS3 works as a feedback inhibitor for a range of cytokine signals and inhibits the function of leptin and downstream steps in the serum lipid levels signaling pathway to regulate energy balance [2-5]. Although this function has been confirmed in animal models, the association data from human studies are relatively limited. Talbert et al. [6] have shown that the SOCS3 is related to body mass index (BMI), visceral adipose, and waist circumference in Hispanic families. However, Jamshidi et al. [7] have shown that the common polymorphism (rs4969168) in SOCS3 is related to body weight, insulin sensitivity or lipid profile between normal female twins. In addition, the study on the association analysis of the polymorphism in the coding sequence and promoter region of the SOCS3 in German children and adolescents with extreme dyslipidemia suggested that no association was observed [8].
China is a multiethnic country. Han nationality is the largest one of 56 ethnic groups, and Mulao nationality is the twenty-ninth largest (with population of 207,352 in 2000) among the 55 minorities. Ninety percent of them live in the Luocheng Mulao Autonomous Country, Guangxi Zhuang Autonomous Region, People’s Republic of China. The history of this minority can be traced back to the Jin Dynasty (AD 265-420). It is well known that the people of Mulao are the descendants of the ancient Baiyue tribe in south China. In a previous study, Xu et al. [9] showed that the genetic relationship between Mulao nationality and other minorities in Guangxi was much closer than that between Mulao and Han or Uighur nationality. To the best of our knowledge, the association between SOCS3 A+930-->G (rs4969168) SNP and serum lipid levels has not been previously explored in the Chinese population. Therefore, the aim of the present study was to detect the association of SOCS3 A+930-->G (rs4969168) SNP and several environmental factors with serum lipid traits in the Han and Mulao populations.
Methods and materials
Participants
Participants in the present study included 690 individuals of Mulao nationality who live in Luocheng Mulao Autonomous County, Guangxi Zhuang Autonomous Region, People’s Republic of China. There were 222 males (32.17%) and 468 females (67.83%). All of them were randomly selected from our previous stratified randomized samples [10]. The ages of the participants ranged from 15 to 93 years, with an average age of 48.40 ± 14.59 years. All of them were rural agricultural workers. In the meantime, a total of 752 Han nationality who reside in the same villages were also randomly selected from our previous stratified randomized samples. The average age of the subjects was 48.79 ± 14.39 years, which ranged from 15 to 84 years. There were 268 men (35.64%) and 484 women (64.36%). All of them were also rural agricultural workers. The whole study subjects were essentially healthy and had no evidence of any chronic illness, including hepatic, renal, or thyroid. The participants with a history of heart attack of myocardial infarction, stroke, congestive heart failure, diabetes or fasting blood glucose ≥ 7.0 mmol/L determined by glucose meter were excluded from the analyses. The participants did not take medications known to affect serum lipid levels (lipid-lowering drugs such as statins or fibrates, beta-blockers, diuretics, or hormones). Ethical approval for this study was obtained from the Ethics Committee of The First Affiliated Hospital, Guangxi Medical University. Written informed consent was provided by all participants.
Epidemiological survey
The survey was carried out using internationally standardized methods [11]. All participants underwent a complete history, physical examination, and laboratory assessment of cardiovascular risk factors. Information on demographics, socioeconomic status, and lifestyle factors was collected with standardized questionnaires. Smoking status was categorized into groups of cigarettes per day: ≤ 20 and > 20. The alcohol information included questions about the number of liang (about 50 g) of rice wine, corn wine, rum, beer, or liquor consumed during the preceding 12 months. Alcohol consumption was categorized into groups of grams of alcohol per day: ≤ 25 and > 25. Sitting blood pressure was measured three times with the use of a mercury sphygmomanometer after the subjects had a 5-minute rest, and the average of the three measurements was used for the level of blood pressure. Systolic blood pressure was determined by the first Korotkoff sound, and diastolic blood pressure was determined by the fifth Korotkoff sound. Body weight, to the nearest 50 grams, was measured by using a portable balance scale. Subjects were weighed without shoes and minimum of clothing. Height was measured, to the nearest 0.5 cm, using a portable measuring device. From these two measurements, BMI (kg/m2) was calculated.
Laboratory methods
A venous blood sample of 5 mL was drawn from all individuals after an overnight (at least 12 hours) fast. The sample was divided into two parts. One part of the sample (2 mL) was collected into glass tube and allowed to clot at room temperature and used to measure serum lipid levels. Another part of the sample (3 mL) was collected into glass tube with anticoagulate solution (4.80 g/L citric acid, 14.70 g/L glucose, and 13.20 g/L tri-sodium citrate) and used to extract DNA. The levels of serum total cholesterol (TC), triglyceride (TG), high-density lipoprotein cholesterol (HDL-C), and low-density lipoprotein cholesterol (LDL-C) in the samples were determined by enzymatic methods with commercially available kits (RANDOX Laboratories Ltd., Ardmore, Diamond Road, Crumlin Co. Antrim, United Kingdom, BT29 4QY; Daiichi Pure Chemicals Co., Ltd., Tokyo, Japan). Serum apolipoprotein (Apo) A1 and ApoB levels were detected by the immunoturbidimetric immunoassay using a commercial kit (RANDOX Laboratories Ltd.). All determinations were performed with an autoanalyzer (Type 7170A; Hitachi Ltd., Tokyo, Japan) in the Clinical Science Experiment Center of The First Affiliated Hospital, Guangxi Medical University [12].
DNA preparation and genotyping
Genomic DNA was isolated from peripheral blood leukocytes using the phenol-chloroform method [10]. The extracted DNA was stored at -20°C until analysis. Genotyping of the SOCS3 A+930-->G (rs4969168) SNP was performed by polymerase chain reaction and restriction fragment length polymorphism (PCR-RFLP). PCR amplification was performed using 5’-CGATGCTATCCGATGAAC-3’ and 5’-TCACTGTAACCTCCACCTC-3’ (Sangon, Shanghai, People’s Republic of China) as the forward and reverse primer pairs; respectively. Each amplification reaction was performed in a total volume of 25 μL reaction mixture, including 100 ng (2 μL) of genomic DNA, 0.75 μL of each primer (10 μmol/L), 12.5 μL 2 × Taq PCR MasterMix (constituent: 0.1 U Taq polymerase/μL, 500 μM dNTP each, 20 mM Tris-HCl, pH 8.3, 100 mM KCL, 3 mM MgCl2, and stabilizers), and 9.0 μL nuclease-free water. After initial denaturizing at 94°C for 5 min, the reaction mixture was subjected to 32 cycles of denaturation at 94°C at 45 s, annealing at 57°C for 35 s and extension 35 s at 72°C, followed by a final 8 min extension at 72°C. After electrophoresis on a 2% agarose gel with 0.5 μg/mL ethidium-bromide, the amplification products were visualized under ultraviolet light. Then the FaqI restriction enzyme of 2.0 U was added directly to the reaction system consisting of PCR products (5 μL), 9 μL of nuclease-free water and 1 μL of 10 × buffer solution and digested at 37°C for 8 hours. After restriction enzyme digestion of the amplified DNA, genotypes were identified by electrophoresis on 2.0% agarose gel and visualized with ethidium-bromide staining ultraviolet illumination. The PCR produced a 437-bp fragment including one FaqI recognition site for the G allele. The G allele can be cleaved whereas the A allele cannot be digested. Therefore, the GG genotype is homozygote for the presence of the site (band at 159- and 99-bp), GA genotype is heterozygote for the absence and presence of the site (bands at 258-, 159- and 99-bp), and AA genotype is homozygote for the absence of the site (bands at 258-bp). Genotypes were scored by an experienced reader blinded to epidemiological data and serum lipid levels. The genotypes detected by PCR-RFLP were also confirmed randomly by direct sequencing (Additional file 1: Figure S1, Sangon Biotech Co., Ltd., Shanghai, People’s Republic of China).
Diagnostic criteria
The normal values of serum TC, TG, HDL-C, LDL-C, ApoA1, ApoB levels and the ratio of ApoA1 to ApoB in our Clinical Science Experiment Center were 3.10-5.17, 0.56-1.70, 1.16-1.42, 2.70-3.10 mmol/L, 1.20-1.60, 0.80-1.05 g/L, and 1.00-2.50; respectively. The individuals with TC > 5.17 mmol/L, and/or TG > 1.70 mmol/L were defined as hyperlipidemic [10]. Hypertension was diagnosed according to the criteria of 1999 World Health Organization-International Society of Hypertension Guidelines for the management of hypertension. Hypertension was defined as an average systolic blood pressure (SBP) ≥ 140 mmHg, and/or an average diastolic blood pressure (DBP) ≥ 90 mmHg, and/or self-reported current treatment for hypertension with antihypertensive medication [13]. The diagnostic criteria of overweight and obesity were according to the Cooperative Meta-analysis Group of China Obesity Task Force. Normal weight, overweight and obesity were defined as a BMI < 24, 24-28, > 28 kg/m2; respectively [14].
Statistical analysis
The statistical analyses were done with the statistical software package SPSS16.0 (SPSS Inc., Chicago, Illinois). Quantitative variables were expressed as mean ± standard deviation (serum TG levels were presented as medians and interquartile ranges). Qualitative variables were expressed as percentages. The difference in general characteristics between two ethnic groups was tested by the Student’s unpaired t-test. Allele frequency was determined via direct counting, and the standard goodness-of-fit test was used to test the Handy-Weinberg equilibrium. Difference in genotype distribution between the groups was obtained using the chi-square test. The association of genotypes and serum lipid parameters was tested by analysis of covariance (ANOVA). Age, sex, BMI, blood pressure, alcohol consumption, cigarette smoking and blood glucose were included in the statistical models as covariates. Multiple linear regression analyses adjusted for age, sex, BMI, blood pressure, alcohol consumption, cigarette smoking and blood glucose were also performed to assess the association of serum lipid levels with genotypes (AA = 0, GA = 1, GG = 2) and several environment factors. A P value of less than 0.05 was considered statistically significant.
Results
General characteristics and serum lipid levels
The baseline characteristics and serum lipid levels of the Han and Mulao populations are presented in Table 1. The levels of weight, BMI, waist circumference, the percentages of alcohol consumption, systolic blood pressure, diastolic blood pressure and pulse pressure, blood glucose were lower in Mulao than in Han (P < 0.05-0.001), whereas the levels of ApoB were higher in Mulao than in Han (P < 0.05). There were no significant differences in the levels of body height, serum TC, TG, HDL-C, LDL-C, ApoA1, the ratio of ApoA1/ApoB, the percentages of cigarette smoking, and age structure between the two ethnic groups (P > 0.05 for all).
Table 1.
Comparison of demographic, lifestyle characteristics and serum lipid levels between the Han and Mulao populations
| Parameter | Han | Mulao | t (X 2) | P |
|---|---|---|---|---|
| Number | 752 | 690 | ||
| Male/female | 268/484 | 222/468 | 1.925 | 0.165 |
| Age (years) | 48.79 ± 14.39 | 48.40 ± 14.59 | 0.521 | 0.602 |
| Height (cm) | 154.22 ± 7.88 | 154.65 ± 7.48 | -1.069 | 0.285 |
| Weight (kg) | 53.16 ± 8.67 | 51.28 ± 8.70 | 4.111 | 0.000 |
| Body mass index (kg/m2) | 22.35 ± 3.36 | 21.40 ± 3.09 | 5.587 | 0.000 |
| waist circumference (cm) | 74.79 ± 7.83 | 73.30 ± 7.89 | 3.600 | 0.000 |
| Cigarette smoking (n%) | ||||
| Nonsmoker | 575 (76.5) | 559 (81.0) | ||
| ≤ 20 cigarettes/day | 149 (19.8) | 113 (16.4) | 4.689 | 0.096 |
| > 20 cigarettes/day | 28 (3.7) | 18 (2.6) | ||
| Alcohol consumption [n (%)] | ||||
| Nondrinker | 611 (81.3) | 578 (83.8) | ||
| ≤ 25 g/day | 67 (8.9) | 38 (5.5) | 6.271 | 0.043 |
| > 25 g/day | 74 (9.8) | 74 (10.7) | ||
| Systolic blood pressure (mmHg) | 127.17 ± 18.37 | 116.84 ± 11.80 | 12.812 | 0.000 |
| Diastolic blood pressure (mmHg) | 81.25 ± 10.77 | 75.46 ± 7.33 | 12.033 | 0.000 |
| Pulse pressure (mmHg) | 45.92 ± 13.79 | 41.38 ± 10.01 | 7.191 | 0.000 |
| Glucose (mmol/L) | 5.95 ± 1.53 | 5.43 ± 0.78 | 8.261 | 0.000 |
| Total cholesterol (mmol/L) | 4.95 ± 1.10 | 4.95 ± 1.27 | -0.124 | 0.901 |
| Triglyceride (mmol/L) | 1.02 (0.76) | 1.01 (0.76) | -1.851 | 0.064 |
| HDL-C (mmol/L) | 1.74 ± 0.58 | 1.78 ± 0.45 | -1.406 | 0.160 |
| LDL-C (mmol/L) | 2.84 ± 0.86 | 2.90 ± 0.89 | -1.301 | 0.193 |
| Apolipoprotein (Apo) A1 (g/L) | 1.34 ± 0.26 | 1.34 ± 0.38 | -0.374 | 0.708 |
| ApoB (g/L) | 0.85 ± 0.20 | 0.94 ± 0.53 | -4.517 | 0.000 |
| ApoA1/ApoB | 1.66 ± 0.48 | 1.67 ± 0.77 | -2.270 | 0.788 |
HDL-C, high-density lipoprotein cholesterol; LDL-C, low-density lipoprotein cholesterol. The quantitative variables were presented as mean ± standard deviation and the difference between the groups was determined by the t-test. The values of triglyceride were presented as median (interquartile range), the difference between the two ethnic groups was determined by the Wilcoxon-Mann-Whitney test. The difference in percentages of cigarette smoking and alcohol consumption between the two ethnic groups was determined by chi-square-test.
Genotypic and allelic frequencies
The genotypic and allelic frequencies of the rs4969168 SNP in the both ethnic groups are shown in Table 2. The frequencies of G and A alleles were 76.20% and 23.80% in Han; and 71.74% and 28.26% in Mulao (P = 0.006); respectively. The frequencies of GG, GA and AA genotypes were 57.71%, 36.97% and 5.32% in Han, and 51.16%, 41.16% and 7.68% in Mulao (P = 0.023); respectively. There was no significant difference in the genotypic and allelic frequencies between males and females in the both ethnic groups (P > 0.05 for all).
Table 2.
Comparison of the genotype and allele frequencies of the tagging SNP A+930-->G of SOCS3 in the Han and Mulao populations [n (%)]
| Group | n | Genotype | Allele | |||
|---|---|---|---|---|---|---|
|
| ||||||
| GG | GA | AA | G | A | ||
| Han | 752 | 434 (57.71) | 278 (36.97) | 40 (5.32) | 1146 (76.20) | 358 (23.80) |
| Mulao | 690 | 353 (51.16) | 284 (41.16) | 53 (7.68) | 990 (71.74) | 390 (28.26) |
| X 2 | – | 7.566 | 7.445 | |||
| P | 0.023 | 0.006 | ||||
| Han | ||||||
| Male | 268 | 154 (57.46) | 99 (36.94) | 15 (5.60) | 407 (75.93) | 129 (24.07) |
| Female | 484 | 280 (57.85) | 179 (36.98) | 25 (5.17) | 739 (76.34) | 229 (23.66) |
| X 2 | 0.065 | 0.032 | ||||
| P | 0.968 | 0.858 | ||||
| Mulao | ||||||
| Male | 222 | 113 (50.90) | 91 (40.99) | 18 (8.11) | 317 (71.40) | 127 (28.60) |
| Female | 468 | 240 (51.28) | 193 (41.24) | 35 (7.48) | 673 (71.90) | 263 (28.10) |
| X 2 | 0.084 | 0.038 | ||||
| P | 0.959 | 0.846 | ||||
Genotypes and serum lipid levels
As shown in Tables 3 and 4, the levels of ApoA1 in Han but not in Mulao were different among the GG, GA and AA genotypes after adjusting age, sex, height, BMI, blood pressure, cigarette smoking, alcohol consumption and blood glucose (P = 0.01), the A allele carriers had lower ApoA1 than the A allele non-carriers. Subgroup analyses showed that the levels of ApoA1 in Han females but not in males were different among the genotypes (P = 0.001), the subjects with AA genotype had lower ApoA1 levels than the subjects with AG or GG genotype. For the Mulao population, the levels of LDL-C and ApoA1 in males but not in females were also different among the genotypes (P < 0.05 for each), the A allele carriers had higher LDL-C and lower ApoA1 levels than the A allele non-carriers.
Table 3.
Comparison of the genotypes and serum lipid levels in the Han and Mulao populations
| Ethnic/Genotype | N | TC (mmol/L) | TG (mmol/L) | HDL-C (mmol/L) | LDL-C (mmol/L) | Apo A1 (g/L) | ApoB (g//L) | ApoA1/ApoB |
|---|---|---|---|---|---|---|---|---|
| Han | 752 | |||||||
| GG | 434 | 4.68 ± 1.40 | 0.98 (0.73) | 1.77 ± 0.57 | 2.82 ± 1.10 | 1.36 ± 0.25 | 0.84 ± 0.19 | 1.68 ± 0.48 |
| GA | 278 | 4.94 ± 1.10 | 1.01 (0.73) | 1.74 ± 0.60 | 2.84 ± 0.82 | 1.34 ± 0.26 | 0.84 ± 0.30 | 1.65 ± 0.48 |
| AA | 40 | 4.99 ± 1.05 | 1.96 (0.77) | 1.57 ± 0.44 | 2.85 ± 0.86 | 1.21 ± 0.30 | 0.85 ± 0.20 | 1.54 ± 0.42 |
| F | 0.425 | 0.217 | 1.639 | 0.005 | 4.591 | 0.310 | 2.194 | |
| P | 0.654 | 0.805 | 0.195 | 0.995 | 0.010 | 0.733 | 0.112 | |
| Mulao | 690 | |||||||
| GG | 353 | 4.85 ± 1.40 | 0.89 (0.66) | 1.79 ± 0.42 | 2.84 ± 0.87 | 1.37 ± 0.39 | 0.85 ± 0.33 | 1.69 ± 0.86 |
| GA | 284 | 5.00 ± 1.43 | 0.97 (0.71) | 1.78 ± 0.48 | 2.94 ± 0.85 | 1.32 ± 0.39 | 0.92 ± 0.56 | 1.68 ± 0.52 |
| AA | 53 | 5.30 ± 1.13 | 1.06 (0.81) | 1.75 ± 0.41 | 3.02 ± 1.22 | 1.32 ± 0.34 | 0.98 ± 0.53 | 1.64 ± 0.71 |
| F | 0.514 | 0.316 | 0.737 | 0.875 | 1.209 | 0.709 | 0.018 | |
| P | 0.598 | 0.729 | 0.479 | 0.417 | 0.299 | 0.493 | 0.982 |
TC, total cholesterol; TG, triglyceride; HDL-C, high-density lipoprotein cholesterol; LDL-C, low-density lipoprotein cholesterol; ApoA1, apolipoprotein A1; ApoB, apolipoprotein B; ApoA1/ApoB, the ratio of apolipoprotein A1 to apolipoprotein B. The value of TG was presented as median (interquartile range). The difference between the genotypes was determined by the Kruskal-Wallis test.
Table 4.
Comparison of the genotypes and serum lipid levels between males and females in the Han and Mulao populations
| Ethnic/Genotype | N | TC (mmol/L) | TG (mmol/L) | HDL-C (mmol/L) | LDL-C (mmol/L) | ApoA1 (g/L) | ApoB (g/L) | ApoA1/ApoB |
|---|---|---|---|---|---|---|---|---|
| Han/male | 268 | |||||||
| GG | 154 | 4.65 ± 1.06 | 1.11 (0.85) | 1.70 ± 0.45 | 2.75 ± 0.90 | 1.39 ± 0.29 | 0.90 ± 0.19 | 1.61 ± 0.49 |
| GA | 99 | 5.20 ± 1.10 | 1.14 (0.76) | 1.67 ± 0.45 | 2.87±0.80 | 1.37 ± 0.30 | 0.91 ± 0.30 | 1.55 ± 0.48 |
| AA | 15 | 5.23 ± 1.07 | 1.26 (0.91) | 1.61 ± 0.34 | 2.95 ± 0.87 | 1.29 ± 0.25 | 0.92 ± 0.21 | 1.51 ± 0.36 |
| F | 1.208 | 0.301 | 0.186 | 0.407 | 0.218 | 0.612 | 0.358 | |
| P | 0.300 | 0.704 | 0.831 | 0.666 | 0.804 | 0.543 | 0.700 | |
| Han/female | 484 | |||||||
| GG | 280 | 4.70 ± 1.60 | 0.96 (0.69) | 1.81 ± 0.62 | 2.79 ± 0.85 | 1.34 ± 0.22 | 0.80 ± 0.30 | 1.73 ± 0.47 |
| GA | 179 | 4.80 ± 1.06 | 0.97 (0.71) | 1.79 ± 0.67 | 2.82 ± 0.83 | 1.32 ± 0.23 | 0.81 ± 0.19 | 1.71 ± 0.47 |
| AA | 25 | 4.85 ± 1.02 | 0.97 (0.72) | 1.54 ± 0.49 | 2.87 ± 1.22 | 1.16 ± 0.32 | 0.81 ± 0.19 | 1.56 ± 0.45 |
| F | 0.040 | 0.222 | 1.806 | 0.174 | 6.913 | 0.039 | 2.193 | |
| P | 0.961 | 0.801 | 0.165 | 0.840 | 0.001 | 0.961 | 0.113 | |
| Mulao/male | 222 | |||||||
| GG | 113 | 4.87 ± 1.87 | 0.87 (0.67) | 1.78 ± 0.46 | 2.76 ± 0.77 | 1.42 ± 0.38 | 0.92 ± 0.20 | 1.63 ± 0.62 |
| GA | 91 | 5.09 ± 1.09 | 1.01 (0.73) | 1.77 ± 0.34 | 2.89 ± 0.83 | 1.26 ± 0.41 | 0.96 ± 0.65 | 1.61 ± 0.83 |
| AA | 18 | 5.34 ± 1.10 | 1.03 (0.81) | 1.70 ± 0.61 | 3.32 ± 0.85 | 1.26 ± 0.36 | 0.99 ± 0.50 | 1.39 ± 0.39 |
| F | 0.967 | 1.093 | 0.189 | 4.249 | 3.056 | 0.094 | 1.954 | |
| P | 0.382 | 0.337 | 0.828 | 0.016 | 0.049 | 0.910 | 0.144 | |
| Mulao/female | 468 | |||||||
| GG | 240 | 4.82 ± 1.56 | 0.95 (0.70) | 1.82 ± 0.41 | 2.86 ± 1.36 | 1.36 ± 0.33 | 0.81 ± 0.37 | 1.83 ± 0.52 |
| GA | 193 | 4.83 ± 1.12 | 1.00 (0.63) | 1.80 ± 0.40 | 2.88 ± 0.92 | 1.35 ± 0.39 | 0.90 ± 0.51 | 1.73 ± 0.88 |
| AA | 35 | 5.01 ± 1.15 | 1.10 (0.81) | 1.74 ± 0.44 | 2.96 ± 0.86 | 1.34 ± 0.37 | 0.97 ± 0.54 | 1.65 ± 0.76 |
| F | 0.328 | 0.784 | 0.355 | 0.010 | 0.089 | 0.794 | 0.467 | |
| P | 0.721 | 0.457 | 0.701 | 0.990 | 0.915 | 0.452 | 0.627 |
TC, total cholesterol; TG, triglyceride; HDL-C, high-density lipoprotein cholesterol; LDL-C, low-density lipoprotein cholesterol; ApoA1, apolipoprotein A1; ApoB, apolipoprotein B; ApoA1/ApoB, the ratio of apolipoprotein A1 to apolipoprotein B. The value of TG was presented as median (interquartile range), the difference was determined by the Kruskal-Wallis test.
Risk factors for serum lipid parameters
The risk factors for serum lipid parameters in Mulao and Han are shown in Tables 5 and 6. Serum lipid parameters were also correlated with several environmental factors such as age, gender, height, weight, BMI, waist circumference, alcohol consumption, cigarette smoking, blood pressure and blood glucose in both ethnic groups (P < 0.05-0.001).
Table 5.
Relationship between serum lipid parameters and relative factors in the Han and Mulao populations
| Lipid parameter | Relative factor | B | Std. error | Beta | t | P |
|---|---|---|---|---|---|---|
| Han and Mulao | ||||||
| TC | Age | 0.013 | 0.002 | 0.153 | 5.789 | 0.000 |
| Alcohol consumption | 0.255 | 0.050 | 0.137 | 5.071 | 0.000 | |
| Height | -0.015 | 0.004 | -0.095 | -3.381 | 0.001 | |
| Waist circumference | 0.025 | 0.004 | 0.167 | 6.244 | 0.000 | |
| Diastolic blood pressure | 0.007 | 0.003 | 0.057 | 2.149 | 0.032 | |
| TG | Alcohol consumption | 0.352 | 0.079 | 0.113 | 4.434 | 0.000 |
| Waist circumference | 0.061 | 0.007 | 0.244 | 9.328 | 0.000 | |
| Diastolic blood pressure | 0.013 | 0.005 | 0.062 | 2.401 | 0.016 | |
| Glucose | 0.080 | 0.040 | 0.051 | 2.012 | 0.044 | |
| HDL-C | Gender | 0.099 | 0.036 | 0.090 | 2.725 | 0.007 |
| Age | 0.003 | 0.001 | 0.080 | 3.035 | 0.002 | |
| Alcohol consumption | 0.129 | 0.025 | 0.158 | 5.073 | 0.000 | |
| Weight | -0.007 | 0.003 | -0.124 | -2.761 | 0.006 | |
| Waist circumference | -0.008 | 0.003 | -0.125 | -3.026 | 0.003 | |
| LDL-C | Ethnic group | 0.102 | 0.045 | 0.058 | 2.278 | 0.023 |
| Age | 0.010 | 0.002 | 0.163 | 6.227 | 0.000 | |
| Height | -0.012 | 0.003 | -0.109 | -4.037 | 0.000 | |
| Waist circumference | 0.022 | 0.003 | 0.196 | 7.442 | 0.000 | |
| ApoA1 | Genotype | 0.027 | 0.013 | 0.051 | 2.012 | 0.044 |
| Gender | 0.087 | 0.025 | 0.127 | 3.496 | 0.000 | |
| Age | 0.002 | 0.001 | 0.108 | 4.024 | 0.000 | |
| Alcohol consumption | 0.147 | 0.016 | 0.288 | 9.281 | 0.000 | |
| Height | 0.004 | 0.001 | 0.098 | 2.823 | 0.005 | |
| Weight | -0.005 | 0.001 | -0.146 | -4.821 | 0.000 | |
| ApoB | Ethnic group | 0.153 | 0.021 | 0.192 | 7.175 | 0.000 |
| Waist circumference | 0.012 | 0.001 | 0.234 | 9.126 | 0.000 | |
| Systolic blood pressure | 0.003 | 0.001 | 0.107 | 3.954 | 0.000 | |
| Glucose | 0.022 | 0.008 | 0.071 | 2.727 | 0.006 | |
| ApoA1/ApoB | Gender | 0.137 | 0.042 | 0.103 | 3.285 | 0.001 |
| Age | -0.002 | 0.001 | -0.054 | -2.080 | 0.038 | |
| Alcohol consumption | 0.129 | 0.030 | 0.131 | 4.263 | 0.000 | |
| Body mass index | -0.025 | 0.007 | -0.128 | -3.611 | 0.000 | |
| Waist circumference | -0.014 | 0.003 | -0.171 | -4.749 | 0.000 | |
| Pulse pressure | -0.003 | 0.001 | -0.062 | -2.328 | 0.020 | |
| Han | ||||||
| TC | Gender | -0.271 | 0.106 | -0.118 | -2.559 | 0.011 |
| Age | 0.010 | 0.003 | 0.134 | 3.701 | 0.000 | |
| Alcohol consumption | 0.278 | 0.071 | 0.160 | 3.913 | 0.000 | |
| Weight | -0.050 | 0.009 | -0.398 | -5.440 | 0.000 | |
| Body mass index | 0.054 | 0.017 | 0.166 | 3.116 | 0.002 | |
| Waist circumference | 0.045 | 0.008 | 0.320 | 5.477 | 0.000 | |
| Diastolic blood pressure | 0.014 | 0.004 | 0.138 | 3.845 | 0.000 | |
| TG | Age | -0.015 | 0.006 | -0.099 | -2.600 | 0.009 |
| Cigarette smoking | 0.824 | 0.149 | 0.198 | 5.520 | 0.000 | |
| Weight | -0.035 | 0.015 | -0.141 | -2.343 | 0.019 | |
| Waist circumference | 0.101 | 0.016 | 0.364 | 6.229 | 0.000 | |
| Diastolic blood pressure | 0.024 | 0.007 | 0.120 | 3.307 | 0.001 | |
| Glucose | 0.162 | 0.051 | 0.114 | 3.158 | 0.002 | |
| HDL-C | Weight | -0.017 | 0.003 | -0.252 | -6.618 | 0.000 |
| Alcohol consumption | 0.114 | 0.035 | 0.124 | 3.248 | 0.001 | |
| LDL-C | Gender | -0.299 | 0.075 | -0.181 | -3.993 | 0.000 |
| Age | 0.012 | 0.002 | 0.194 | 5.432 | 0.000 | |
| Cigarette smoking | -0.299 | 0.075 | -0.181 | -3.993 | 0.000 | |
| Height | -0.019 | 0.005 | -0.176 | -4.102 | 0.000 | |
| Waist circumference | 0.021 | 0.004 | 0.195 | 5.421 | 0.000 | |
| ApoA1 | Age | 0.001 | 0.001 | 0.075 | 2.215 | 0.027 |
| Height | -0.009 | 0.001 | -0.290 | -7.953 | 0.000 | |
| Cigarette smoking | 0.050 | 0.020 | 0.100 | 2.504 | 0.012 | |
| Alcohol consumption | 0.138 | 0.017 | 0.336 | 8.242 | 0.000 | |
| ApoB | Gender | -0.069 | 0.019 | -0.161 | -3.638 | 0.000 |
| Age | 0.001 | 0.001 | 0.088 | 2.495 | 0.013 | |
| Alcohol consumption | 0.035 | 0.012 | 0.109 | 2.829 | 0.005 | |
| Height | -0.005 | 0.001 | -0.190 | -4.818 | 0.000 | |
| Waist circumference | 0.009 | 0.001 | 0.346 | 10.147 | 0.000 | |
| Diastolic blood pressure | 0.002 | 0.001 | 0.110 | 3.232 | 0.001 | |
| Glucose | 0.016 | 0.004 | 0.119 | 3.563 | 0.000 | |
| ApoA1/ApoB | Gender | 0.233 | 0.046 | 0.224 | 4.805 | 0.000 |
| Age | -.003 | 0.001 | -0.096 | -2.919 | 0.004 | |
| Cigarette smoking | 0.137 | 0.041 | 0.151 | 3.380 | 0.001 | |
| Alcohol consumption | 0.111 | 0.031 | 0.148 | 3.594 | 0.000 | |
| Body mass index | -0.030 | 0.006 | -0.212 | -4.744 | 0.000 | |
| Waist circumference | -0.014 | 0.003 | -0.236 | -5.131 | 0.000 | |
| Mulao | ||||||
| TC | Age | 0.012 | 0.003 | 0.139 | 3.709 | 0.000 |
| Waist circumference | 0.023 | 0.006 | 0.144 | 3.872 | 0.000 | |
| Pulse pressure | 0.009 | 0.005 | 0.074 | 1.974 | 0.049 | |
| TG | Cigarette smoking | -0.318 | 0.154 | -0.086 | -2.073 | 0.039 |
| Alcohol consumption | 0.433 | 0.113 | 0.160 | 3.840 | 0.000 | |
| Waist circumference | 0.047 | 0.008 | 0.216 | 5.831 | 0.000 | |
| Glucose | -0.175 | 0.082 | -0.079 | -2.073 | 0.039 | |
| HDL-C | Gender | 0.126 | 0.043 | 0.133 | 2.940 | 0.003 |
| Age | 0.003 | 0.001 | 0.086 | 2.357 | 0.019 | |
| Alcohol consumption | 0.115 | 0.031 | 0.166 | 3.738 | 0.000 | |
| Body mass index | -0.026 | 0.008 | -0.178 | -3.369 | 0.001 | |
| Waist circumference | -0.006 | 0.003 | -0.112 | -2.109 | 0.035 | |
| LDL-C | Age | 0.009 | 0.002 | 0.151 | 4.082 | 0.000 |
| Alcohol consumption | -0.103 | 0.052 | -0.074 | -1.997 | 0.046 | |
| Body mass index | 0.049 | 0.011 | 0.170 | 4.576 | 0.000 | |
| ApoA1 | Gender | 0.167 | 0.045 | 0.203 | 3.729 | 0.000 |
| Age | 0.003 | 0.001 | 0.121 | 3.004 | 0.003 | |
| Alcohol consumption | 0.138 | 0.027 | 0.230 | 5.062 | 0.000 | |
| Height | 0.005 | 0.003 | 0.105 | 2.093 | 0.037 | |
| ApoB | Waist circumference | 0.015 | 0.002 | 0.224 | 6.071 | 0.000 |
| Pulse pressure | 0.006 | 0.002 | 0.112 | 3.042 | 0.002 | |
| ApoA1/ApoB | Waist circumference | -0.019 | 0.004 | -0.198 | -5.310 | 0.000 |
| Pulse pressure | -0.007 | 0.003 | -0.089 | -2.387 | 0.017 |
TC, total cholesterol; TG, triglyceride; HDL-C, high-density lipoprotein cholesterol; LDL-C, low-density lipoprotein cholesterol; ApoA1, apolipoprotein A1; ApoB, apolipoprotein B; ApoA1/ApoB, the ratio of apolipoprotein A1 to apolipoprotein B.
Table 6.
Relationship between serum lipid parameters and relative factors in the males and females of the Han and Mulao populations
| Lipid parameter | Relative factor | B | Std. error | Beta | t | P |
|---|---|---|---|---|---|---|
| Han/male | ||||||
| TC | Alcohol consumption | 0.251 | 0.076 | 0.194 | 3.322 | 0.001 |
| Diastolic blood pressure | 0.027 | 0.006 | 0.267 | 4.606 | 0.000 | |
| Glucose | 0.090 | 0.038 | 0.138 | 2.376 | 0.018 | |
| TG | Weight | -0.094 | 0.036 | -0.272 | -2.608 | 0.010 |
| Cigarette smoking | 0.711 | 0.286 | 0.143 | 2.487 | 0.014 | |
| Waist circumference | 0.196 | 0.040 | 0.510 | 4.896 | 0.000 | |
| HDL-C | Alcohol consumption | 0.105 | 0.031 | 0.201 | 3.406 | 0.001 |
| Cigarette smoking | 0.086 | 0.040 | 0.123 | 2.125 | 0.035 | |
| Weight | -0.016 | 0.003 | -0.340 | -5.818 | 0.000 | |
| Diastolic blood pressure | 0.007 | 0.002 | 0.167 | 2.882 | 0.004 | |
| LDL-C | Body mass index | 0.030 | 0.013 | 0.139 | 2.352 | 0.019 |
| Cigarette smoking | -0.300 | 0.079 | -0.226 | -3.822 | 0.000 | |
| ApoA1 | Cigarette smoking | 0.080 | 0.025 | 0.174 | 3.184 | 0.002 |
| Alcohol consumption | 0.132 | 0.019 | 0.382 | 6.843 | 0.000 | |
| Weight | -0.009 | 0.002 | -0.270 | -4.900 | 0.000 | |
| Diastolic blood pressure | 0.004 | 0.001 | 0.153 | 2.801 | 0.005 | |
| ApoB | Alcohol consumption | 0.35 | 0.014 | 0.144 | 2.573 | 0.011 |
| Height | -0.004 | 0.002 | -0.161 | -2.752 | 0.006 | |
| Waist circumference | 0.008 | 0.001 | 0.320 | 5.380 | 0.000 | |
| Diastolic blood pressure | 0.003 | 0.001 | 0.156 | 2.716 | 0.007 | |
| Glucose | 0.019 | 0.007 | 0.158 | 2.815 | 0.005 | |
| ApoA1/ApoB | Body mass index | -0.028 | 0.008 | -0.231 | -3.432 | 0.001 |
| Alcohol consumption | 0.106 | 0.032 | 0.190 | 3.342 | 0.001 | |
| Cigarette smoking | 0.146 | 0.042 | 0.197 | 3.496 | 0.001 | |
| Waist circumference | -0.011 | 0.004 | -0.195 | -2.911 | 0.004 | |
| Han/female | ||||||
| TC | Age | 0.022 | 0.004 | 0.273 | 6.233 | 0.000 |
| Waist circumference | 0.025 | 0.006 | 0.164 | 3.978 | 0.000 | |
| Height | -0.038 | 0.008 | -0.202 | -4.636 | 0.000 | |
| TG | Diastolic blood pressure | 0.017 | 0.005 | 0.144 | 3.319 | 0.001 |
| Waist circumference | 0.053 | 0.008 | 0.301 | 6.912 | 0.000 | |
| Glucose | 0.106 | 0.037 | 0.121 | 2.878 | 0.004 | |
| HDL-C | Age | 0.005 | 0.002 | 0.100 | 2.196 | 0.029 |
| Weight | -0.014 | 0.004 | -0.143 | -3.134 | 0.002 | |
| LDL-C | Age | 0.020 | 0.003 | 0.306 | 6.935 | 0.000 |
| Waist circumference | 0.022 | 0.005 | 0.182 | 4.370 | 0.000 | |
| Height | -0.019 | 0.007 | -0.123 | -2.802 | 0.005 | |
| ApoA1 | Age | 0.002 | 0.001 | 0.116 | 2.591 | 0.010 |
| Weight | -0.009 | 0.002 | -0.248 | -5.656 | 0.000 | |
| Alcohol consumption | 0.195 | 0.064 | 0.133 | 3.031 | 0.003 | |
| ApoB | Age | 0.002 | 0.001 | 0.110 | 2.312 | 0.021 |
| Height | -0.005 | 0.001 | -0.140 | -3.317 | 0.001 | |
| Waist circumference | 0.009 | 0.001 | 0.340 | 8.473 | 0.000 | |
| Systolic blood pressure | 0.002 | 0.001 | 0.136 | 2.963 | 0.003 | |
| Glucose | 0.013 | 0.006 | 0.096 | 2.303 | 0.022 | |
| ApoA1/ApoB | Age | -0.003 | 0.002 | -0.095 | -2.106 | 0.036 |
| Alcohol consumption | 0.303 | 0.120 | 0.105 | 2.525 | 0.012 | |
| Body mass index | -0.029 | 0.010 | -0.183 | -2.832 | 0.005 | |
| Waist circumference | -0.017 | 0.004 | -0.253 | -3.902 | 0.000 | |
| Pulse pressure | -0.005 | 0.002 | -0.132 | -3.003 | 0.003 | |
| Mulao/male | ||||||
| TC | Weight | 0.041 | 0.012 | 0.226 | 3.440 | 0.001 |
| TG | Weight | 0.062 | 0.020 | 0.205 | 3.102 | 0.002 |
| HDL-C | Alcohol consumption | 0.136 | 0.038 | 0.235 | 3.609 | 0.000 |
| Body mass index | -0.042 | 0.012 | -0.224 | -3.444 | 0.001 | |
| LDL-C | Body mass index | 0.057 | 0.020 | 0.191 | 2.893 | 0.004 |
| ApoA1 | Genotype | 0.093 | 0.039 | 0.149 | 2.371 | 0.019 |
| Age | 0.004 | 0.002 | 0.147 | 2.354 | 0.019 | |
| Alcohol consumption | 0.142 | 0.028 | 0.319 | 5.085 | 0.000 | |
| ApoB | Body mass index | 0.049 | 0.013 | 0.247 | 3.807 | 0.000 |
| Pulse pressure | 0.009 | 0.004 | 0.154 | 2.381 | 0.018 | |
| ApoA1/ApoB | Body mass index | -0.061 | 0.016 | -0.243 | -3.712 | 0.000 |
| Alcohol consumption | 0.155 | 0.051 | 0.199 | 3.035 | 0.003 | |
| Pulse pressure | -0.009 | 0.005 | -0.128 | -1.975 | 0.050 | |
| Mulao/female | ||||||
| TC | Age | 0.017 | 0.004 | 0.208 | 4.565 | 0.000 |
| Waist circumference | 0.014 | 0.007 | 0.092 | 2.061 | 0.040 | |
| Pulse pressure | 0.011 | 0.005 | 0.095 | 2.095 | 0.037 | |
| TG | Alcohol consumption | 1.056 | 0.324 | 0.144 | 3.232 | 0.001 |
| Waist circumference | 0.041 | 0.007 | 0.247 | 5.558 | 0.000 | |
| HDL-C | Age | 0.003 | 0.001 | 0.104 | 2.364 | 0.018 |
| Body mass index | -0.021 | 0.008 | -0.170 | -2.597 | 0.010 | |
| Waist circumference | -0.008 | 0.003 | -0.157 | -2.393 | 0.017 | |
| LDL-C | Age | 0.013 | 0.003 | 0.202 | 4.519 | 0.000 |
| Waist circumference | 0.020 | 0.005 | 0.163 | 3.649 | 0.000 | |
| ApoA1 | Genotype | 0.029 | 0.015 | 0.096 | 1.972 | 0.049 |
| Age | 0.003 | 0.001 | 0.150 | 2.020 | 0.044 | |
| Body mass index | -0.125 | 0.048 | -1.678 | -2.603 | 0.010 | |
| ApoB | Waist circumference | 0.014 | 0.003 | 0.213 | 4.769 | 0.000 |
| Glucose | 0.097 | 0.029 | 0.149 | 3.327 | 0.001 | |
| ApoA1/ApoB | Age | -0.007 | 0.003 | -0.128 | -2.843 | 0.005 |
| Waist circumference | -0.020 | 0.005 | -0.192 | -4.251 | 0.000 |
TC, total cholesterol; TG, triglyceride; HDL-C, high-density lipoprotein cholesterol; LDL-C, low-density lipoprotein cholesterol; ApoA1, apolipoprotein A1; ApoB, apolipoprotein B; ApoA1/ApoB, the ratio of apolipoprotein A1 to apolipoprotein B.
Discussion
In the current study, we showed that serum lipid profiles were significantly different between males and females in both Han and Mulao ethnic groups. As expect, the levels of associated risk factors were lower in Mulao than in Han, whereas the serum levels of bad apolipoprotein were higher in Mulao than in Han. A significant difference in the genotype and allele frequencies of SOCS3 A+930-->G (rs4969168) SNP was also noted between the Han and Mulao populations. The minor A allele frequencies in Han and Mulao were 23.80% and 28.26% respectively, which were in close proximity to those of Chinese Han Beijing (27.9%) reported in international haplotype map (HapMap) project [15]. On gender subgroup analysis, there were no significant differences in the genotypic and allelic frequencies between males and females in the both ethnic groups. According to HapMap data, the minor allele frequency of SOCS3 A+930-->G (rs4969168) SNP was 32.6% in Japanese, and 72.6% in Inbadab Yoruba and Utahns. Apparently, the minor allele frequency was lower in Asian than the Western populations. These findings suggest that genotype and allele frequencies of SOCS3 A+930-->G (rs4969168) SNP are inconsistent among diverse ethnic groups.
With the release of data from the HapMap phase III project and completion of several whole genome association studies on several common diseases realized that tagSNPs in target genes could be selected as candidate loci to cover all of the polymorphisms involved in the haploblocks of the target gene. SOCS3 is one of several genes involved in cytokine signaling and regulates the function of proteins downstream, inhibits the insulin signaling pathway and stimulates the upregulation of TNF-α in adipose tissue [14]. The protein encoded by SOCS3 is also important in energy balance and regulation [2-5]. This result has been confirmed in animal models, but the association data in humans have been relatively limited. Another potential explanation is that different haploblock distributions appear in different ethnic groups or in different nationalities. Consequently, pathogenic loci linked to tagSNPs can be partially or totally different, and in some cases, special ethnic tagSNPs would lose their ability of catching pathogenic loci in other ethnic studies, which seems to have happened in our study. Therefore, our results are reasonable given that SOCS3 serves as both a pivotal and hub function in a complex regulatory system, which further suggests that SOCS3 may also play a dual role in regulating serum lipid levels.
A recent meta-analysis reported that SOCS3 A+930-->G (rs4969168) SNP lack of association SNP with metabolism in Germany [16]. SOCS3 genes induced by leptin resistance may lead to obesity patients lipoprotein enzyme activity decreased, the levels of TG reduce, will eventually cause high TG, LDL-C [17] and low HDL-C [18,19]. In the present study, serum ApoA1 levels in Han females, and LDL-C and ApoA1 levels in Mulao males were different among the three genotypes, the A allele carriers had lower ApoA1 and higher LDL-C levels than the A allele non-carriers. The reason for this discrepancy is not fully understood. It might be due the differences in genetic backgrounds, diebits, and environmental factors between the two ethnic populations and/or simple due to the low power of this study. It is well accepted that ethnic differences in serum lipid levels were partly due to the differences in the dietary intakes [20,21]. Diet alone could account for up to 2.5% of the variability on serum lipid levels [22-26]. Although rice and corn are the staple foods for both ethnic groups; Mulao peoples have a typical habit of eating cold foods along with acidic and spicy dishes, local bean soy sauce, pickled vegetables and animal offal’s which contain abundant saturated fatty acid. Therefore, it is possible that the difference in dietary habit between Mulao and Han ethnic groups partly contribute variability in the effect of SOCS3 A+930-->G (rs4969168) SNP on serum lipid levels. To the best of our knowledge, this study is the first attempt to report the association between SOCS3 A+930-->G (rs4969168) SNP and serum lipid levels in Han and Mulao population including our previous studies [27-30]. Therefore, further studies with larger sample size are still needed to confirm this association.
Several environmental factors were also correlated with serum lipid levels of both Mulao and Han populations. In the current study, the levels of weight, BMI, waist circumference, the percentages of alcohol consumption, systolic blood pressure, diastolic blood pressure and pulse pressure, blood glucose were lower in Mulao than in Han, whereas the levels of ApoB were higher in Mulao than in Han. Garcia Palmieri et al. stated that diet and relative weight could account for up to 6% of the variability in serum cholesterol levels [22]. In particular, for every 1 kg decrease in body weight, TG decreased by 0.011 mmol/L and HDL-C increased by 0.011 mmol/L [31]. Rimm et al. documented that consuming of 30 g of ethanol per day increased the concentrations of HDL-C by 3.99 mg/dl, ApoA1 by 8.82 mg/dl, and TG by 5.69 mg/dl [32]. Yin et al. also showed that BMI, cigarette smoking and alcohol consumption could interact with certain lipid-related gene variants to modify the serum lipid levels in Bai Ku Yao and Han Chinese ethnic groups [33,34]. Therefore, the results of exposure to different environmental factors may further modify the effect of genetic variation on serum lipid levels in our study populations.
There are some potential limitations in our study. First, it is undeniable that this study has insufficient power to produce a robust conclusion; therefore, such a small scale study needs to replicate in independent cohorts. Second, the cross-sectional study design limits the ability to determine any causality of the relationships observed. Third, the impact of diet was not evaluated in this study. It is possible that part of the relationship observed in this study may be partly influenced by the effect of dietary intake.
In Conclusion, the present study showed that the distribution of genotype and allele frequencies and the association of SOCS3 A+930-->G (rs4969168) SNP serum lipid levels were significantly different between the Han and Mulao populations. These results suggest that there may be a racial/ethnic-and/or sex-specific association between the SOCS3 A+930-->G (rs4969168) SNP and serum lipid parameters in some ethnic groups.
Acknowledgements
This study was supported by the National Natural Science Foundation of China (No: 30960130).
Disclosure of conflict of interest
None.
Supporting Information
References
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