Hypertension. 2002;40:609-611
Published online before print October 7, 2002, doi: 10.1161/01.HYP.0000036448.44066.53
Published online before print October 7, 2002, doi: 10.1161/01.HYP.0000036448.44066.53
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(Hypertension. 2002;40:609.)
© 2002 American Heart Association, Inc.
Hypothesis Paper |
Angiotensin Blockade Prevents Type 2 Diabetes by Formation of Fat Cells
From HELIOS Klinikum Berlin, Franz Volhard Clinic–Charité, Humboldt University of Berlin, and Max Delbrück Center for Molecular Medicine, Berlin, Germany.
Correspondence to Arya M. Sharma, MD, Canada Research Chair for Cardiovascular Obesity Research and Management, McMaster University, Hamilton, Ontario L8L 2X2, Canada. E-mail sharma{at}ccc.mcmaster.ca
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.
Key Words: angiotensin • diabetes • adipose tissue • insulin resistance • obesity
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