Obesity Research Center, The University of Tennessee, Knoxville, TN 37996-4588, USA.
Obes Rev. 2012 Feb;13(2):136-49. doi: 10.1111/j.1467-789X.2011.00942.x. Epub 2011 Oct 31.
The renin-angiotensin system (RAS) is classically known for its role in regulation of blood pressure, fluid and electrolyte balance. Recently, several local RASs in organs such as brain, heart, pancreas and adipose tissue have also been identified. Evidence from clinical trials suggests that in addition to anti-hypertensive effects, pharmacological inhibition of RAS also provides protection against the development of type-2 diabetes. Moreover, animal models with targeted inactivation of RAS genes exhibit improved insulin sensitivity and are protected from high-fat diet-induced obesity and insulin resistance. Because there is evidence for RAS overactivation in obesity, it is possible that RAS is a link between obesity and insulin resistance. This review summarizes the evidence and mechanistic insights on the associations between RAS, obesity and insulin resistance, with special emphasis on the role of adipose tissue RAS in the pathogenesis of metabolic derangements in obesity.
肾素-血管紧张素系统（RAS）经典地被认为在调节血压、液体和电解质平衡方面发挥作用。最近，在脑、心脏、胰腺和脂肪组织等器官中也发现了几种局部 RAS。临床试验的证据表明，除了抗高血压作用外，RAS 的药理学抑制还能提供对 2 型糖尿病发展的保护。此外，靶向 RAS 基因失活的动物模型表现出改善的胰岛素敏感性，并能防止高脂肪饮食引起的肥胖和胰岛素抵抗。由于肥胖存在 RAS 过度激活的证据，因此 RAS 可能是肥胖和胰岛素抵抗之间的联系。这篇综述总结了 RAS、肥胖和胰岛素抵抗之间关联的证据和机制见解，特别强调了脂肪组织 RAS 在肥胖代谢紊乱发病机制中的作用。
