Zhang Y, Wat N, Stratton I M, Warren-Perry M G, Orho M, Groop L, Turner R C
Diabetes Research Laboratories, Radcliffe Infirmary, Oxford, UK.
Diabetologia. 1996 Dec;39(12):1505-11. doi: 10.1007/s001250050605.
Insulin receptor substrate-1 (IRS-1), beta 3-adrenergic-receptor (beta 3-AR) and glycogen synthase (GS) genes are candidate genes for non-insulin-dependent diabetes mellitus (NIDDM), insulin resistance, dyslipidaemia and obesity. We studied white Caucasian subjects with NIDDM, 227 being randomly selected, 49 NIDDM within the top two percentiles of insulin resistance; 54 with dyslipidaemia in the top quintile of triglyceride/insulin and the bottom quintile of HDL, and 166 non-diabetic control subjects. We examined the association of the simple tandem repeat DNA polymorphisms (STRPs) near the IRS-1 and GS genes, and the prevalence of mutations at codons of IRS-1 513 and 972, beta 3-AR 64 and GS 464 using restriction fragment length polymorphism (RFLP). The STRP alleles in IRS-1 were significantly different between NIDDM and control subjects (p = 0.015). The IRS-1 972 mutation was significantly different between the four groups with increased prevalence in the insulin resistant and dyslipidaemia subjects (18 and 26% compared with 11% in control subjects; p < 0.0005). Those with or without IRS-1 mutations had similar clinical characteristics and impaired insulin sensitivity. beta 3-AR 64 mutation was not significantly different between the four groups but those with the mutation were more obese, with a test for linear association between number of alleles and degree of obesity in an analysis of variance showing a significant association (p = 0.029). The GS 464 mutation was not detected in any of the diabetic or control subjects and the population association study using GS STRP showed no difference in allelic frequencies between NIDDM patients and control subjects. A mutation in lipoprotein lipase at codon 291, associated in the general population with low HDL cholesterol, was not at increased prevalence in the NIDDM patients with dyslipidaemia. In conclusion, IRS-1 972 had an increased prevalence in subjects with insulin resistance, with or without dyslipidaemia. beta 3-AR 64 was associated with increased obesity but not with insulin resistance or dyslipidaemia. These separate contributions to different features of NIDDM are an example of the polygenic inheritance of this heterogeneous disorder.
胰岛素受体底物-1(IRS-1)、β3-肾上腺素能受体(β3-AR)和糖原合酶(GS)基因是非胰岛素依赖型糖尿病(NIDDM)、胰岛素抵抗、血脂异常和肥胖的候选基因。我们研究了患有NIDDM的白种人受试者,随机选取了227例,其中49例NIDDM患者处于胰岛素抵抗前两个百分位;54例血脂异常患者处于甘油三酯/胰岛素前五分位且高密度脂蛋白处于后五分位,以及166例非糖尿病对照受试者。我们检测了IRS-1和GS基因附近的简单串联重复DNA多态性(STRP)的关联,以及使用限制性片段长度多态性(RFLP)检测IRS-1 513和972、β3-AR 64和GS 464密码子处的突变发生率。NIDDM患者和对照受试者之间IRS-1中的STRP等位基因存在显著差异(p = 0.015)。IRS-1 972突变在四组之间存在显著差异,在胰岛素抵抗和血脂异常受试者中的发生率增加(分别为18%和26%,而对照受试者为11%;p < 0.0005)。有或没有IRS-1突变的患者具有相似的临床特征和胰岛素敏感性受损。β3-AR 64突变在四组之间无显著差异,但有该突变的患者更肥胖,在方差分析中对等位基因数量与肥胖程度之间的线性关联检验显示存在显著关联(p = 0.029)。在任何糖尿病或对照受试者中均未检测到GS 464突变,使用GS STRP进行的群体关联研究显示NIDDM患者和对照受试者之间等位基因频率无差异。在一般人群中与低高密度脂蛋白胆固醇相关的脂蛋白脂肪酶291密码子处的突变,在患有血脂异常的NIDDM患者中发生率并未增加。总之,IRS-1 972在有或无血脂异常的胰岛素抵抗受试者中发生率增加。β3-AR 64与肥胖增加相关,但与胰岛素抵抗或血脂异常无关。这些对NIDDM不同特征的单独作用是这种异质性疾病多基因遗传的一个例子。