Two Common Polymorphisms of PPARγ Gene in patients with Metabolic Syndrome in an Iranian population

Background and Aims: Peroxisome proliferator-activated receptor-γ (PPARγ), is a nuclear hormone receptor, serves as a master regulator of genes involved in adipocyte differentiation, lipid metabolism, glucose homeostasis, and could be a genetic risk factor for metabolic syndrome (MetS). The aim of this study was to investigate possible association between the C1431T and Pro12Ala genetic variants of PPARγ gene and risk of MetS in an Iranian population. Methods: A total of 200 subjects comprised of 100 individuals with criteria for the MetS and 100 healthy subjects were genotyped by TaqMan real time PCR, using DNA extracted from collected blood samples by commercial kits. Each group was then divided into two subgroups according to genotype (CC and CT + TT for C1431T, Pro/Pro and Pro/Ala + Ala/Ala for Pro12Ala). Anthropometric measurements, fasting glucose and lipid profile were measured by standard methods. Results: Frequencies of C1431T genotypes, but not Pro12Ala, were significantly different between MetS and control group. For C1431T polymorphism frequency of the T allele (p = 0.001: OR = 0.42: 95% CI = 0.21-0.82) and genotypes carrying mutant allele (CT +TT) (p = 0.02: OR= 0.44: 95% CI = 0.2-0.89) were significantly more in MetS group. In stratified analyses for Pro12Ala, Ala carriers in subjects with age < 50 years, had lower total cholesterol (p < 0.03) and in subjects with age > 50 years, had decreased central obesity (p < 0.003). Conclusions: Our results suggest that C1431T, but not Pro12Ala polymorphisms, may be associated with MetS. Although there was no evidence that Pro12Ala polymorphism might be significantly associated with the metabolic syndrome, a weak protective effect of this variant with metabolic syndrome related parameters including total cholesterol and central obesity cannot be ignored. Further association studies with larger population are needed to arrive at any definite conclusions.

PPARγ, Polymorphism, Metabolic syndrome, Genotype