EFFECT OF THE Pro12Ala POLYMORPHISM OF THE PEROXISOME PROLIFERATOR-ACTIVATED RECEPTOR γ2 GENE ON LIPID PROFILE AND ADIPOKINES LEVELS IN OBESE SUBJECTS
Becer E1,2,*, Çırakoğlu A3
*Corresponding Author: Eda Becer, Ph.D., M.Sc., Department of Biochemistry, Faculty of Pharmacy, Near East University, Nicosia, Mersin 10, Turkey. Tel: +90-392-680-2000, Ext: 128. Fax:+90-392-680-2038. E-mail: edabecer@yahoo.com
page: 71

RESULTS

Descriptive statistics of anthropometric and metabolic characteristics of the study population are presented in Table 1. Obese and non obese subjects did not differ in age, while plasma glucose, total cholesterol, triglycerides, LDL-cholesterol, leptin, chemerin and resistin levels (p <0.001) were significantly higher, and mean HDL-cholesterol (p <0.001) levels were significantly lower in obese than in non obese subjects. Non obese subjects had significantly higher adiponectin levels and lower HOMA-IR than obese subjects (p <0.001). Analysis of the PPARγ2 gene yielded three variants of the genotype: PP (wild-type), PA (heterozygous), and AA (homozygous). The PPARγ2 genotype frequencies were calculated and are presented in Table 2. In obese subjects, the genotype frequencies were 61.25% for PP, 26.87% for PA, and 11.87% for AA. The frequencies of PP, PA and AA genotypes were 57.86, 35.0, and 7.14%, respectively, in non obese subjects. There was no significant derivation of genotypic distribution from HWE in non obese subjects (χ2 = 0.46, p = 0.61). However, The PPARγ2 genotype frequencies appear to be in HWE (χ2 = 13.38, p = 0.0051) in the obese group. The deficit of the PA genotype frequencies in obese subjects probably accounts for the deviation from HWE. The PPARγ2 allele frequencies were calculated and are presented in Table 2. The proline allele of PPARγ2 (found in 74.69% of obese subjects and 75.36% of non obese subjects) and the alanine allele (found in 24.64% of non obese subjects and 25.31% of obese subjects) did not differ between obese and non obese subjects (p = 0.92). There was no difference in age, BMI, HOMA-IR, waist or hip circumference, serum glucose, total cholesterol, LDLcholesterol, HDL-cholesterol, triglycerides, adiponectin, resistin or leptin levels between the three genotypes in non obese subjects. The PPARγ2 Pro12Ala polymorphism showed significant association with leptin (p <0.001) and chemerin (p <0.047) levels in non obese subjects (Table 3). A post hoc analysis with Tukey’s test for multiple comparisons revealed no significant difference between the leptin level mean values of AA and PA genotypes (p >0.05). However, a significant difference was found between the mean values of the PP and PA genotypes and the PP and AA genotypes (p <0.05). Post hoc analyses of the chemerin level means showed significant differences between the PP and AA genotypes, while the mean values of the AA and PA genotypes did not differ significantly in non obese subjects. The PPARγ2 Pro12Ala polymorphism showed a significant association with triglycerides (p <0.046), leptin (p <0.001), chemerin (p = 0.002), adiponectin (p = 0.01) and resistin (p <0.001) levels in obese subjects. The homozygous AA subjects’ triglyceride values were significantly higher than the heterozygote PA and homozygote PP obese subjects. Post hoc comparisons showed that AA homozygotes had higher triglyceride mean values than those with the PP genotype (p <0.05). Obese homozygous AA subjects showed significantly higher levels of leptin (p <0.001) than those with the homozygous PP genotype and heterozygous PA genotype. Post hoc comparisons in obese subjects showed that AA homozygotes had significantly higher mean values than PP and PA, while no significant difference was found between the mean values of the PP and PA genotypes (p >0.05). Additionally, obese subjects carrying an A allele showed significantly lower adiponectin levels (p = 0.01) than homozygous subjects with the P allele. Post hoc comparisons showed that AA homozygotes had lower adiponectin mean values than those with the PP genotype. The level of resistin was lower in obese subjects carrying a P allele. The post hoc analysis with Tukey’s test for multiple comparisons revealed significant differences between the resistin mean values of PP and PA genotypes and the PP and AA genotypes (p <0.05). However, no significant difference was found between the mean values of the AA and PA genotypes (p >0.05). The wild-type PP subjects’ chemerin values were significantly lower than the heterozygous PA and homozygous AA obese subjects. Post hoc comparisons in obese subjects showed that PP wild-type had significantly lower mean values than PA and AA, while no significant difference was found between the mean values of the PP and PA genotypes (p >0.05). No significant differences in age, BMI, waist or hip circumference, HOMA-IR, serum glucose, HDL-cholesterol, LDLcholesterol, total cholesterol levels were observed between the three genotypes in obese subjects (Table 3).



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