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

BackgroundAdiponectin, 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. MethodsWe 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. ResultsSignificant 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. ConclusionsThe 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.