Linking Adiponectin Gene Variants (+45T>G and +276G>T) to Adipokine Levels and Metabolic Syndrome in a North Indian Adult Women

Abstract

Background: Adiponectin, an adipocyte-derived adipokine, is often downregulated in obesity-related disorders. This study aimed to explore the association between adiponectin gene variants (+45T>G, rs2241766, and +276G>T, rs1501299) and circulating adipokine levels as well as metabolic syndrome in North Indian adult women. Methods: We genotyped single nucleotide polymorphisms (SNPs) in 541 adult women, comprising 269 with metabolic syndrome (MetS) according to NCEP-ATP III criteria and 272 without MetS (wMetS; control). We assessed circulating levels of adiponectin, leptin, lipid profile, glucose, insulin, and HOMA-IR. Results: Significant differences (p<0.01) were observed in circulating adipokines (adiponectin and leptin), lipid profile, glucose, insulin, HOMA-IR, and waist-to-hip ratio (WHR) between wMetS and MetS women. The frequency of the combined mutant genotype (TG+GG) at +45T>G was significantly lower (p=0.017) in MetS women, while the mutant G allele was higher (p=0.008) compared to the wild type. For the +276G>T variant, the frequency of the mutant T allele was significantly lower (p=0.027) in MetS women compared to wMetS women. The mutant genotypes GG of +45T>G and TT of +276G>T were significantly associated with lower adiponectin levels, higher leptin levels, and increased HOMA-IR (all p<0.001) in MetS women. Conclusions: The findings suggest that adiponectin gene variants (+45T>G and +276G>T), along with reduced adiponectin levels and elevated HOMA-IR, may contribute significantly to the development of metabolic syndrome.