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首页> 外文期刊>Life sciences >Adiponectin and peroxisome proliferator-activated receptor-γ gene polymorphisms and gene-gene interactions with type 2 diabetes
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Adiponectin and peroxisome proliferator-activated receptor-γ gene polymorphisms and gene-gene interactions with type 2 diabetes

机译：脂联素和过氧化物酶体增殖物激活受体-γ基因多态性与2型糖尿病的基因-基因相互作用

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Aims To investigate whether gene polymorphisms of both adiponectin and peroxisome proliferator-activated receptor gamma (PPARγ) influence type 2 diabetes mellitus (T2DM) respectively in the Han people of the Wenzhou region of China and whether the interaction of gene polymorphism between adiponectin and PPARγ influences T2DM in the same subjects. Main methods This study included 198 patients with T2DM and 255 healthy individuals. Polymerase chain reaction-restriction fragment length polymorphism analyses were used to detect single nucleotide polymorphisms (SNPs). Logistic regression and multifactor dimensionality reduction (MDR) methods were used to analyze gene-gene interactions. Key findings The frequency distribution of adiponectin SNP11377 was not different (p = 0.792), but the frequency of CC, CG and GG genotypes showed the difference between two groups (T2DM: 57.1%, 33.3%, and 9.6%; control: 53.7%, 41.6%, and 4.7%, respectively; p = 0.047). Adiponectin SNP45, SNP276 and PPAR γ SNPp12a were equally distributed between the two groups (p = 0.586, 0.119, 0.437, respectively), and there were no significant differences in genotype frequencies between the two groups (p = 0.751, 0.144, 0.479, respectively). Linkage disequilibrium existed between SNP11377 and SNP45 (p < 0.001) and SNP45 and SNP276 (p < 0.001). Haplotype analyses showed no significant differences between the T2DM and control groups. According to the logistic regression and MDR gene-gene interaction analyses, SNP11377GG and SNP276GT interactions increased the risk of T2DM (odds ratio = 6.984, p = 0.012). Significance Adiponectin SNP11377 and SNP276 gene-gene interactions are associated with the increased risk of T2DM in this population.
机译：目的探讨脂联素和过氧化物酶体增殖物激活受体γ（PPARγ）的基因多态性是否分别影响中国温州地区汉族的2型糖尿病（T2DM），以及脂联素和PPARγ之间的基因多态性是否相互影响T2DM中的相同主题。主要方法该研究纳入198例T2DM患者和255例健康个体。聚合酶链反应-限制性片段长度多态性分析用于检测单核苷酸多态性（SNP）。 Logistic回归和多因素降维（MDR）方法用于分析基因-基因相互作用。主要发现脂联素SNP11377的频率分布没有差异（p = 0.792），但CC，CG和GG基因型的频率显示两组之间的差异（T2DM：57.1％，33.3％和9.6％;对照组：53.7％）。 ，分别为41.6％和4.7％; p = 0.047）。脂联素SNP45，SNP276和PPARγSNPp12a在两组之间均等分布（分别为p = 0.586、0.119、0.437），两组之间的基因型频率无显着差异（分别为p = 0.751、0.144、0.479 ）。 SNP11377和SNP45（p <0.001）和SNP45和SNP276（p <0.001）之间存在连锁不平衡。单倍型分析显示T2DM与对照组之间无显着差异。根据逻辑回归和MDR基因-基因相互作用分析，SNP11377GG和SNP276GT相互作用增加了T2DM的风险（优势比= 6.984，p = 0.012）。意义脂联素SNP11377和SNP276基因-基因相互作用与该人群中T2DM的风险增加有关。

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