Stumvoll Michael, Häring Hans
University Hospital, Department of Endocrinology, Metabolism and Pathobiochemistry, Eberhard-Karls-Universität, Tübingen, Germany.
Diabetes. 2002 Aug;51(8):2341-7. doi: 10.2337/diabetes.51.8.2341.
Peroxisome proliferator-activated receptor (PPAR)-gamma is a transcription factor with a key role in adipocyte differentiation. The Ala allele of the common Pro12Ala polymorphism in the isoform PPAR-gamma2 is associated with reduced risk for type 2 diabetes. The effect on the individual is weak, but because of a prevalence of >75% of the high-risk Pro allele, the population-attributable risk is enormous. The in vivo effects of the polymorphism are secondary to alterations in adipose tissue, where PPAR-gamma2 is predominantly expressed. Moderate reduction in transcriptional activity of PPAR-gamma as a result of the polymorphism modulates production and release of adipose-derived factors. Both decreased release of insulin-desensitizing free fatty acids, tumor necrosis factor-alpha, and resistin and increased release of the insulin-sensitizing hormone adiponectin result in secondary improvement of insulin sensitivity of glucose uptake and suppression of glucose production. The population effect of this polymorphism may be modulated by environmental or genetic factors such as obesity, ethnicity, ratio of unsaturated to saturated fatty acids, and genetic background. Once diabetes has developed, the protective effect of the Ala allele may be lost, since increased vascular complications and more pronounced beta-cell dysfunction have been reported. These observations, however, are currently unexplained. In conclusion, the Pro12Ala polymorphism in PPAR-gamma2 represents the first genetic variant with a broad impact on the risk of common type 2 diabetes. The precise understanding of its mechanism may lead to novel diagnostic, preventive, and therapeutic approaches for improving the management of type 2 diabetes.
过氧化物酶体增殖物激活受体(PPAR)-γ是一种在脂肪细胞分化中起关键作用的转录因子。PPAR-γ2亚型中常见的Pro12Ala多态性的Ala等位基因与2型糖尿病风险降低相关。对个体的影响较弱,但由于高危Pro等位基因的患病率>75%,人群归因风险巨大。该多态性的体内效应继发于脂肪组织的改变,PPAR-γ2主要在脂肪组织中表达。由于该多态性导致PPAR-γ转录活性适度降低,调节了脂肪源性因子的产生和释放。胰岛素脱敏游离脂肪酸、肿瘤坏死因子-α和抵抗素的释放减少以及胰岛素增敏激素脂联素的释放增加,均导致葡萄糖摄取的胰岛素敏感性继发性改善和葡萄糖生成的抑制。这种多态性的人群效应可能受环境或遗传因素调节,如肥胖、种族、不饱和脂肪酸与饱和脂肪酸的比例以及遗传背景。一旦糖尿病发生,Ala等位基因的保护作用可能丧失,因为已有报道称血管并发症增加和β细胞功能障碍更明显。然而,目前这些观察结果尚无法解释。总之,PPAR-γ2中的Pro12Ala多态性是首个对常见2型糖尿病风险有广泛影响的基因变异。对其机制的精确理解可能会带来改善2型糖尿病管理的新诊断、预防和治疗方法。