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Angiotensin-(1-7) Mas-receptor deficiency decreases peroxisome proliferator-activated receptor gamma expression in adipocytes

Item Type:Article
Title:Angiotensin-(1-7) Mas-receptor deficiency decreases peroxisome proliferator-activated receptor gamma expression in adipocytes
Creators Name:Mario, E.G. and Santos, S.H.S. and Ferreira, A.V.M. and Bader, M. and Santos, R.A.S. and Botion, L.M.
Abstract:The renin-angiotensin system is an important link between metabolic syndrome and cardiovascular diseases. Besides angiotensin II, other angiotensin peptides such as angiotensin-(1-7), have important biological activities. It has been demonstrated that angiotensin-(1-7), acting through the G protein-coupled receptor encoded by the Mas protooncogene have important actions on the cardiovascular system. However, the role of angiotensin-(1-7)-Mas axis in lipidic profile is not well established. In the present study, the adipocyte metabolism was investigated in wild type and FVB/N Mas-deficient male mice. The gene expression of peroxisome proliferator-activated receptor gamma, acetyl-CoA carboxylase and the amount of fatty acid synthase protein were reduced in the Mas-knockout mice. Serum nonesterified fatty acids of Mas-knockout showed a 50% increase in relation to wild type group. Basal and isoproterenol-stimulated lipolysis was similar between the groups, however, a significant decrease of the glycerol release (lipolytic index) in response to insulin was observed in wild type animals, while no effect of the insulin action was observed in a Mas-knockout group. The data suggest that the lack of angiotensin-(1-7) action through Mas receptor alters the response of adipocytes to insulin action. These effects might be related to decreased expression of PPARgamma.
Keywords:Acetyl-CoA Carboxylase, Adipocytes, Adipose Tissue, Fatty Acid Synthetase Complex, Gene Expression Regulation, Glycerol, G-Protein-Coupled Receptors, Insulin, Isoproterenol, Knockout Mice, Lipolysis, Nonesterified Fatty Acids, PPAR gamma, Proto-Oncogene Proteins, Animals, Mice
Source:Peptides
ISSN:0196-9781
Publisher:Elsevier (U.S.A.)
Volume:33
Number:1
Page Range:174-177
Date:January 2012
Official Publication:https://doi.org/10.1016/j.peptides.2011.11.014
PubMed:View item in PubMed

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