TRB3基因+251A/G多态性与糖耐量减低的关系
Correlation of TRB3+251A/G Polymorphism with Impaired Glucose Tolerance
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摘要:
目的 分析TRB3 基因+251A/G多态性分布,并探讨该多态性与糖耐量减低(IGT)及胰岛素抵抗的相关性。 方法 在112 例IGT 者和209 例对照者中,采用Taqman 探针方法对TRB3 基因+251A/G 位点进行基因分型;同时进行问卷调查、体格检查及血糖、血脂、胰岛素等生化指标的检测,并计算稳态模型法β 细胞功能指数(HOMA-B)、早期相胰岛素分泌指数(ΔI30/ΔG30)、稳态模型法胰岛素抵抗指数(HOMA-IR)、Cederholm胰岛素敏感指数(ISIc)等评价胰岛素分泌及胰岛素敏感性。 结果 在IGT 组与对照组中,性别、年龄差异无统计学意义;两组临床指标比较:BMI、血糖(空腹及糖后2 h)、糖化血红蛋白、游离脂肪酸、胰岛素(空腹及糖后2 h)、ΔI30/ΔG30、HOMA-IR、ISIc 等10 项差异有统计学意义。TRB3 基因+251A/G位点存在多态性。AA、AG、GG 3 种基因型的频率分布在IGT 组、对照组分别为64.29%、64.11%,28.57%、32.54%,7.14%、3.35%,其分布差异无统计学意义(χ2=0.006,P=0.938)。两组不同基因型的临床指标比较:在IGT 组中, AG/GG基因型者空腹胰岛素、HOMA-IR高于 AA基因型者(P<0.05);对照组+251A/G不同基因型者血糖、血脂、胰岛素、HOMA-B、HOMA-IR等各指标差异均无统计学意义。 结论 TRB3 基因+251A/G多态性与研究人群IGT 的发生无关,但可能与IGT 者肝脏胰岛素抵抗存在相关性。 Abstract:Objective To describe the polymorphism distribution of TRB3 + 251A/G, and to identify its correlation with impaired glucose tolerance (IGT) and insulin resistance. Methods A total of 112 IGT subjects and 209 control subjects were genotyped by Taqman probe method. Questionnaire survey, physical examination, and biochemical measurements of glucose, lipid, and insulin were conducted. Homeostasis model assessment for β-cell function index (HOMA-B), index of early phase insulin secretion (ΔI30/ΔG30), homeostasis model assessment for insulin resistance index (HOMA-IR), insulin sensitivity index by Cederholm (ISIc) were calculated to assess insulin release and insulin sensitivity. Results In comparison between the IGT and control groups, there was no statistical difference in gender or age, but differences were observed in 10 tested indicators, including body mass index, glucose (0 h and 2 h), hemoglobin A1c, free fatty acids, insulin (0 h and 2 h), ΔI30/ΔG30, HOMA-IR, and ISIc. The gene polymorphisms of TRB3 + 251A/G were identified．The frequencies of AA,AG,GG were 64.29%, 28.57%, and 7.14% genotypes in the IGT group versus 64.11%, 32.54%, and 3.35% in the control group respectively, and there was no significant difference (χ2=0.006,P=0.938). In comparison of clinical characteristics, the participants with IGT carrying AG/GG versus those carrying AA showed higher levels of insulin (0 h) and HOMA-IR (P<0.05); no significant difference was observed in glucose, lipid, insulin, HOMA-B, or HOMA-IR between AA and AG/GG genotypes in the controls. Conclusion TRB3 + 251A/G polymorphism is not associated with IGT in the studied population. However, it might be correlated with liver insulin resistance among IGT subjects.
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