Clausen J O, Hansen T, Bjørbaek C, Echwald S M, Urhammer S A, Rasmussen S, Andersen C B, Hansen L, Almind K, Winther K
Steno Diabetes Center, Gentofte, Denmark.
Lancet. 1995 Aug 12;346(8972):397-402. doi: 10.1016/s0140-6736(95)92779-4.
We previously discovered two aminoacid polymorphisms in codons 513 and 972 of the protein insulin receptor substrate-1 (IRS-1), which is important in cellular insulin action. We have investigated whether these polymorphisms are associated with changes in insulin sensitivity in a random sample of young healthy adults. Insulin sensitivity and secretion were measured during a combined intravenous glucose and tolbutamide tolerance test in 380 unrelated white subjects aged 18-32. IRS-1 polymorphisms were examined by single-strand conformation polymorphism and verified by restriction-enzyme digestion. No homozygous carrier of the codon-513 variant was identified, but one non-obese man had the codon-972 mutation on both alleles. He had low fasting-serum insulin and C-peptide concentrations and low insulin sensitivity and glucose effectiveness. During a 24 h dexamethasone test, he developed transient diabetes. In their heterozygous forms the codon-513 and codon-972 variants of IRS-1 were found in 3% and 9% of the subjects. Non-obese carriers of either polymorphism had similar insulin sensitivity and pancreatic beta-cell function to non-obese wild-type subjects (no known variants of IRS-1). Analysis of variance showed, however, a significant interaction between obesity (body-mass index > or = 25 kg/m2) and the heterozygous form of the codon-972 variant (p < 0.003); obese polymorphism carriers had lower insulin sensitivity than obese non-carriers (mean 6.0 [SD 3.3] vs 12.3 [9.5] x 10(-5) L min-1 pmol-1). The obese carriers of the codon-972 variant were also characterised by a clustering of metabolic cardiovascular risk factors, with raised fasting concentrations of plasma glucose, serum triglyceride, and plasma tissue-plasminogen-activator and its fast-acting inhibitor. With adjustment for known modulators of insulin sensitivity, multivariate analyses showed that the combination of obesity and the codon-972 variant was associated with a 50% reduction in insulin sensitivity (p = 0.0008). Our results suggest that the codon-972 IRS-1 gene variant may interact with obesity in the pathogenesis of common insulin-resistant disorders.
我们先前在胰岛素受体底物-1(IRS-1)蛋白的513和972密码子中发现了两个氨基酸多态性,该蛋白在细胞胰岛素作用中起重要作用。我们在一组随机抽取的年轻健康成年人中研究了这些多态性是否与胰岛素敏感性的变化相关。在一项联合静脉葡萄糖和甲苯磺丁脲耐量试验中,对380名年龄在18至32岁之间的无亲缘关系的白人受试者测量了胰岛素敏感性和分泌。通过单链构象多态性检测IRS-1多态性,并通过限制性酶切进行验证。未发现513密码子变体的纯合携带者,但有一名非肥胖男性两个等位基因均有972密码子突变。他的空腹血清胰岛素和C肽浓度较低,胰岛素敏感性和葡萄糖有效性也较低。在一项24小时地塞米松试验中,他出现了短暂性糖尿病。在3%和9%的受试者中发现了IRS-1的513密码子和972密码子变体的杂合形式。任一多态性的非肥胖携带者与非肥胖野生型受试者(无已知IRS-1变体)具有相似的胰岛素敏感性和胰岛β细胞功能。然而,方差分析显示,肥胖(体重指数≥25kg/m²)与972密码子变体的杂合形式之间存在显著交互作用(p<0.003);肥胖多态性携带者的胰岛素敏感性低于肥胖非携带者(平均值分别为6.0[标准差3.3]和12.3[9.5]×10⁻⁵L·min⁻¹·pmol⁻¹)。972密码子变体的肥胖携带者还具有代谢心血管危险因素聚集的特征,空腹血浆葡萄糖、血清甘油三酯、血浆组织型纤溶酶原激活剂及其快速作用抑制剂浓度升高。在对已知的胰岛素敏感性调节因子进行校正后,多变量分析显示,肥胖与972密码子变体的组合与胰岛素敏感性降低50%相关(p = 0.0008)。我们的结果表明,972密码子IRS-1基因变体可能在常见胰岛素抵抗性疾病的发病机制中与肥胖相互作用。