Angiotensin-(1–7) Mas-receptor deficiency decreases peroxisome proliferator-activated receptor gamma expression in adipocytes
Peptides, ISSN: 0196-9781, Vol: 33, Issue: 1, Page: 174-177
2012
- 37Citations
- 26Captures
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Metrics Details
- Citations37
- Citation Indexes37
- 37
- CrossRef32
- Captures26
- Readers26
- 26
Article Description
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 PPARγ.
Bibliographic Details
http://www.sciencedirect.com/science/article/pii/S0196978111005018; http://dx.doi.org/10.1016/j.peptides.2011.11.014; http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=84855819598&origin=inward; http://www.ncbi.nlm.nih.gov/pubmed/22119778; https://linkinghub.elsevier.com/retrieve/pii/S0196978111005018; https://dx.doi.org/10.1016/j.peptides.2011.11.014
Elsevier BV
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