Angiotensin-(1-7) suppresses oxidative stress and improves glucose uptake via Mas receptor in adipocytes View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

2012-08

AUTHORS

Chang Liu, Xiao-Hong Lv, Hong-Xing Li, Xi Cao, Fen Zhang, Lei Wang, Mei Yu, Jin-Kui Yang

ABSTRACT

Although reactive oxygen species (ROS) contribute to glucose intolerance induced by the renin-angiotensin system (RAS) is well documented, the role of the newly discovered pathway of RAS, angiotensin (Ang)-(1-7)/Mas axis, in this process remains unknown. Here, we examined the effect of Ang-(1-7) on oxidative stress and glucose uptake in adipocytes. We used primary cultured epididymal adipocytes from C57 mice to study Ang-(1-7) effects on glucose uptake. We also treated fully differentiated 3T3-L1 adipocytes with exogenous Ang-(1-7) or overexpression of angiotensin-converting enzyme 2 (ACE2) to induce endogenous generation of Ang-(1-7) to clarify its effects on ROS production. Intracellular ROS was measured by flow cytometry, dihydroethidium (DHE), and nitroblue tetrazolium assay. Levels of NADPH oxidase and adiponectin mRNA were measured by real-time PCR. Ang-(1-7) improved glucose uptake both in basal and insulin-stimulated states. ROS production was slightly but significantly decreased in adipocytes treated with Ang-(1-7). Additionally, Mas receptor antagonist D-Ala7-Ang-(1-7) (A779) reversed the effect of Ang-(1-7) on glucose uptake and oxidative stress. Furthermore, treatment of adipocytes with Ang-(1-7) decreased NADPH oxidase mRNA levels. We also found that oxidative stress induced by glucose oxidase-suppressed expression of adiponectin, an insulin-sensitive protein. However, the suppression of oxidative stress by Ang-(1-7) restored adiponectin expression, while A779 agonists these changes induced by Ang-(1-7). In conclusion, Ang-(1-7) can protect against oxidative stress and improve glucose metabolism in adipocytes. These results show that Ang-(1-7) is a novel target for the improvement of glucose metabolism by preventing oxidative stress. More... »

PAGES

291-299

Identifiers

URI

http://scigraph.springernature.com/pub.10.1007/s00592-011-0348-z

DOI

http://dx.doi.org/10.1007/s00592-011-0348-z

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1043243449

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/22042130


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