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首页> 外文期刊>Genetic Testing >Gene-Gene Interactions Among Genetic Variants from Obesity Candidate Genes for Nonobese and Obese Populations in Type 2 Diabetes
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Gene-Gene Interactions Among Genetic Variants from Obesity Candidate Genes for Nonobese and Obese Populations in Type 2 Diabetes

机译：2型糖尿病非肥胖和肥胖人群的肥胖候选基因的遗传变异之间的基因-基因相互作用。

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摘要

Recent studies indicate that obesity may play a key role in modulating genetic predispositions to type 2 diabetes (T2D). This study examines the main effects of both single-locus and multilocus interactions among genetic variants in Taiwanese obese and nonobese individuals to test the hypothesis that obesity-related genes may contribute to the etiology of T2D independently and/or through such complex interactions. We genotyped 11 single nucleotide polymorphisms for 10 obesity candidate genes including adrenergic beta-2-receptor surface, adrenergic beta-3-receptor surface, angiotensinogen, fat mass and obesity associated gene, guanine nucleotide binding protein beta polypeptide 3 (GNB3), interleukin 6 receptor, proprotein convertase subtilisin/kexin type 1 (PCSK1), uncoupling protein 1, uncoupling protein 2, and uncoupling protein 3. There were 389 patients diagnosed with T2D and 186 age- and sex-matched controls. Single-locus analyses showed significant main effects of the GNB3 and PCSK1 genes on the risk of T2D among the nonobese group (p = 0.002 and 0.047, respectively). Further, interactions involving GNB3 and PCSK1 were suggested among the nonobese population using the generalized multifactor dimensionality reduction method (p = 0.001). In addition, interactions among angiotensinogen, fat mass and obesity associated gene, GNB3, and uncoupling protein 3 genes were found in a significant four-locus generalized multifactor dimensionality reduction model among the obese population (p = 0.001). The results suggest that the single nucleotide polymorphisms from the obesity candidate genes may contribute to the risk of T2D independently and/or in an interactive manner according to the presence or absence of obesity.
机译：最近的研究表明，肥胖可能在调节2型糖尿病（T2D）的遗传易感性中起关键作用。这项研究研究了台湾肥胖和非肥胖个体的遗传变异之间单基因座和多基因座相互作用的主要影响，以检验肥胖相关基因可能独立和/或通过这种复杂相互作用导致T2D病因的假设。我们对10个肥胖候选基因（包括肾上腺素β-2-受体表面，肾上腺素β-3受体表面，血管紧张素原，脂肪量和肥胖症相关基因，鸟嘌呤核苷酸结合蛋白β多肽3（GNB3），白介素6）的11个单核苷酸多态性进行了基因分型。受体，前蛋白转化酶枯草杆菌蛋白酶/ kexin 1型（PCSK1），解偶联蛋白1，解偶联蛋白2和解偶联蛋白3。共有389例被诊断为T2D的患者和186个年龄和性别匹配的对照。单基因座分析显示，非肥胖组中GNB3和PCSK1基因对T2D风险有重大的主要影响（分别为p = 0.002和0.047）。此外，建议使用广义多因素降维方法在非肥胖人群中涉及GNB3和PCSK1的相互作用（p = 0.001）。此外，在肥胖人群中一个重要的四位通用多因素降维模型中，发现了血管紧张素原，脂肪量和肥胖相关基因，GNB3和解偶联蛋白3基因之间的相互作用（p = 0.001）。结果表明，来自肥胖候选基因的单核苷酸多态性可能根据肥胖的存在或不存在独立和/或以交互方式导致T2D的风险。

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  • 来源
    《Genetic Testing》 |2009年第4期|485-493|共9页
  • 作者

    Eugene Lin; Dee Pei; Yi-Jen Huang; Chang-Hsun Hsieh; Lawrence Shih-Hsin Wu;

  • 作者单位

    Bioinformatics Division, Vita Genomics, Inc., Taipei County, Taiwan;

    Division of Endocrinology and Metabolism, Cardinal Tien Hospital, Taipei County, Taiwan;

    Division of Endocrinology and Metabolism, Tri-Service General Hospital, Taipei, Taiwan;

    Division of Endocrinology and Metabolism, Tri-Service General Hospital, Taipei, Taiwan;

    Research Development Division, Vita Genomics, Inc., Taipei County, Taiwan Research Development Division Vita Genomics, Inc.7Fl., No. 6, Section 1 Jungshing Road Wugu Shiang Taipei County 248 Taiwan;

  • 收录信息 美国《科学引文索引》(SCI);美国《化学文摘》(CA);
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