BHF Glasgow Cardiovascular Research Centre, University of Glasgow, 126 University Place, Glasgow G11 6TA, United Kingdom.
Biochem Pharmacol. 2011 Feb 15;81(4):471-7. doi: 10.1016/j.bcp.2010.11.010. Epub 2010 Nov 25.
The rapid rise in prevalence of type 2 diabetes mellitus (T2DM) has been driven by changes in environmental factors - primarily increased caloric intake and reduced energy expenditure - resulting in reduced whole body insulin sensitivity (often termed insulin resistance). Insulin resistance has been proposed to be a major driver of progression to T2DM. However, of 38 individual susceptibility loci for T2DM recently identified by genome wide association studies, by far the majority code for proteins involved in β-cell function. In this review, we discuss the possible reasons for the paucity of insulin resistance genes and ask whether the new genetic susceptibility data should focus attention on β-cell targets in the development of therapies for T2DM.
2 型糖尿病（T2DM）患病率的迅速上升是由环境因素的变化引起的，主要是热量摄入增加和能量消耗减少，导致全身胰岛素敏感性降低（通常称为胰岛素抵抗）。胰岛素抵抗被认为是导致 T2DM 进展的主要驱动因素。然而，在最近通过全基因组关联研究确定的 38 个 T2DM 个体易感性基因座中，绝大多数编码的是参与β细胞功能的蛋白质。在这篇综述中，我们讨论了胰岛素抵抗基因缺乏的可能原因，并探讨了新的遗传易感性数据是否应该将注意力集中在β细胞靶点上，以开发治疗 T2DM 的疗法。
