Lack of interaction between angiotensin II and angiotensin (1‐7) on lipid metabolism from isolated adipocytes

The renin‐angiotensin system is an important link between cardiovascular diseases and obesity. It is well known that angiotensin II (Ang II) is consequently related with obesity and G‐protein coupled receptor Mas, an essential mediator of angiotensin‐(1‐7) [Ang‐(1‐7)], deficient mouse leads to dramatic change inducing metabolic syndrome. However, the role of Ang‐(1‐7) which counteracts Ang II functions is not thoroughly known. The aim of present study is to define the interaction between Ang II and Ang‐(1‐7) on the lipid metabolism using isolated adipocyte s from rodent and human visceral adipose tissues. Isoproterenol (10 −7 , 10 −6 , 10 −5 M) induced an increase in glycerol release in a dose‐dependent manner in the adipocytes isolated from rat epididymal and human visceral adipose tissues. Ang II (10 −7 , 10 −6 , 10 −5 M) did not cause any change of lipolysis by itself However, the pretreatment with Ang II reduced glycerol release induced by with isoproterenol (10 −6 M) in both types of isolated adipocytes. No differences in inhibition of isoproterenol‐induced lipolysis by Ang II was found between large and small size of human adipocytes Ang‐(1‐7) (10 −8 , 10 −7 , 10 −6 M) did not show any change in lipolysis by itself. In addition, the pretreatment with Ang‐(1‐7) did not modify any effects of Ang II and isoproterenol on lipolysis. Ang II (10 −8 , 10 −7 , 10 −6 M) induced preadipocyte differentiation in 3T3‐L1 cells, whereas Ang‐(1‐7) did not change growth and differentiation compared with control preadipocytes. These results suggest that Ang‐(1‐7) does not appear to have counterbalance with Ang II in the lipid metabolism of adipocytes isolated from rat and human adipose tissues. Supported by the KOSEF (R13‐2008‐005‐‐0).