title: Angiotensin blockade prevents type 2 diabetes by formation of fat cells.
abstract: 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.
authors.affiliation: HELIOS Klinikum Berlin, Franz Volhard Clinic-Charité, Humboldt University of Berlin, and Max Delbrück Center for Molecular Medicine, Berlin, Germany. sharma@ccc.mcmaster.ca
authors.forename: Arya M
authors.initials: AM
authors.lastname: Sharma
authors.forename: Jürgen
authors.initials: J
authors.lastname: Janke
authors.forename: Kerstin
authors.initials: K
authors.lastname: Gorzelniak
authors.forename: Stefan
authors.initials: S
authors.lastname: Engeli
authors.forename: Friedrich C
authors.initials: FC
authors.lastname: Luft
mesh_terms: D017667:Adipocytes / Q000166:cytology / Q000187:drug effects / Q000378:metabolism*; D000804:Angiotensin II / Q000037:antagonists & inhibitors* / Q000096:biosynthesis / Q000494:pharmacology; D057911:Angiotensin Receptor Antagonists; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000494:pharmacology; D000818:Animals; D001562:Benzimidazoles / Q000494:pharmacology; D001565:Benzoates / Q000494:pharmacology; D002454:Cell Differentiation / Q000187:drug effects; D002986:Clinical Trials as Topic / Q000706:statistics & numerical data; D003920:Diabetes Mellitus / Q000503:physiopathology; D003924:Diabetes Mellitus, Type 2 / Q000209:etiology / Q000503:physiopathology / Q000517:prevention & control*; D004195:Disease Models, Animal; D006801:Humans; D007004:Hypoglycemic Agents / Q000494:pharmacology; D007333:Insulin Resistance / Q000502:physiology; D009765:Obesity; D044140:Receptor, Angiotensin, Type 1; D012084:Renin-Angiotensin System / Q000187:drug effects / Q000502:physiology; D000077333:Telmisartan
chemical_list: D057911:Angiotensin Receptor Antagonists; D000806:Angiotensin-Converting Enzyme Inhibitors; D001562:Benzimidazoles; D001565:Benzoates; D007004:Hypoglycemic Agents; D044140:Receptor, Angiotensin, Type 1; D000804:Angiotensin II; D000077333:Telmisartan