Diabetes Center, Department of Internal Medicine, VU University Medical Center, Amsterdam, The Netherlands.
Diabetes Obes Metab. 2012 Jul;14(7):586-95. doi: 10.1111/j.1463-1326.2012.01559.x. Epub 2012 Feb 13.
Agents interfering with the renin-angiotensin system (RAS) were consistently shown to lower the incidence of type 2 diabetes mellitus (T2DM), as compared to other antihypertensive drugs, in hypertensive high-risk populations. The mechanisms underlying this protective effect of RAS blockade using angiotensin-converting enzyme inhibitors or angiotensin-receptor blockers on glucose metabolism are not fully understood. In this article, we will review the evidence from randomized controlled trials and discuss the proposed mechanisms as to how RAS interference may delay the onset of T2DM. In particular, as T2DM is characterized by β-cell dysfunction and obesity-related insulin resistance, we address the mechanisms that underlie RAS blockade-induced improvement in β-cell function and insulin sensitivity.
血管紧张素转换酶抑制剂或血管紧张素受体阻滞剂阻断肾素-血管紧张素系统（RAS）可降低高血压高危人群 2 型糖尿病（T2DM）的发生率，优于其他降压药物。但 RAS 阻断对葡萄糖代谢的这种保护作用的机制尚不完全清楚。本文将综述随机对照试验的证据，并讨论 RAS 干预如何延迟 T2DM 发病的可能机制。特别是，由于 T2DM 的特征是β细胞功能障碍和肥胖相关的胰岛素抵抗，我们探讨了 RAS 阻断引起的β细胞功能和胰岛素敏感性改善的机制。
