Sharma Arya M, Janke Jürgen, Gorzelniak Kerstin, Engeli Stefan, Luft Friedrich C
HELIOS Klinikum Berlin, Franz Volhard Clinic-Charité, Humboldt University of Berlin, and Max Delbrück Center for Molecular Medicine, Berlin, Germany.
Hypertension. 2002 Nov;40(5):609-11. doi: 10.1161/01.hyp.0000036448.44066.53.
Obesity is the prime risk factor for the development of type 2 diabetes. Recent clinical trials have shown that blockade of the renin-angiotensin system, either by inhibiting the angiotensin-converting enzyme or blocking the angiotensin type 1 receptor, may substantially lower the risk for type 2 diabetes. The mechanism underlying this effect is unknown. Based on our recent observation that angiotensin II markedly inhibits adipogenic differentiation of human adipocytes via the angiotensin type I receptor and that expression of angiotensin II-forming enzymes in adipose tissue is inversely correlated with insulin sensitivity, we propose the hypothesis that blockade of the renin-angiotensin system prevents diabetes by promoting the recruitment and differentiation of adipocytes. Increased formation of adipocytes would counteract the ectopic deposition of lipids in other tissues (muscle, liver, pancreas), thereby improving insulin sensitivity and preventing the development of type 2 diabetes.
肥胖是2型糖尿病发生的主要危险因素。最近的临床试验表明，通过抑制血管紧张素转换酶或阻断血管紧张素1型受体来阻断肾素-血管紧张素系统，可能会大幅降低2型糖尿病的风险。这种效应背后的机制尚不清楚。基于我们最近的观察，即血管紧张素II通过血管紧张素I型受体显著抑制人脂肪细胞的脂肪生成分化，且脂肪组织中血管紧张素II生成酶的表达与胰岛素敏感性呈负相关，我们提出假说：阻断肾素-血管紧张素系统可通过促进脂肪细胞的募集和分化来预防糖尿病。脂肪细胞形成增加将抵消脂质在其他组织（肌肉、肝脏、胰腺）中的异位沉积，从而改善胰岛素敏感性并预防2型糖尿病的发生。
