将北印度成年女性的脂肪连接素基因变异(+45T>G 和 +276G>T)与脂肪因子水平和代谢综合征联系起来

Abhishek Gupta, Arun Kumar Singh, Priyanka Gupta, Vani Gupta
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摘要

背景:脂联素是一种来源于脂肪细胞的脂肪因子,在肥胖相关疾病中经常被下调。本研究旨在探讨北印度成年女性的脂肪连通素基因变异(+45T>G,rs2241766 和 +276G>T,rs1501299)与循环脂肪因子水平以及代谢综合征之间的关联:我们对 541 名成年女性的单核苷酸多态性(SNPs)进行了基因分型,其中包括根据 NCEP-ATP III 标准患有代谢综合征(MetS)的 269 名女性和未患有代谢综合征(wMetS;对照组)的 272 名女性。我们评估了脂肪连素、瘦素、血脂、血糖、胰岛素和 HOMA-IR 的循环水平:结果:在循环脂肪因子(脂联素和瘦素)、血脂、血糖、胰岛素、HOMA-IR 和腰臀比(WHR)方面,wMetS 和 MetS 女性之间存在显著差异(p<0.01)。与野生型相比,MetS女性中+45T>G的组合突变基因型(TG+GG)的频率明显较低(p=0.017),而突变的G等位基因则较高(p=0.008)。就+276G>T变体而言,与wMetS女性相比,MetS女性中突变T等位基因的频率明显较低(p=0.027)。在MetS女性中,+45T>G的突变基因型GG和+276G>T的突变基因型TT与较低的脂肪连素水平、较高的瘦素水平和较高的HOMA-IR显著相关(均为p<0.001):研究结果表明,脂肪连通素基因变异(+45T>G 和 +276G>T)以及脂肪连通素水平降低和 HOMA-IR 升高可能是代谢综合征发病的重要原因。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Linking Adiponectin Gene Variants (+45T>G and +276G>T) to Adipokine Levels and Metabolic Syndrome in a North Indian Adult Women
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.
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