Lack of weight gain after angiotensin AT1 receptor blockade in diet-induced XXXX is partly mediated by an angiotensin-(1-7)/Mas-dependent pathway.

@entity4689 @entity353 @entity28 @entity72115 @entity35 @entity9887
BACKGROUND AND PURPOSE: Angiotensin AT1 receptor antagonists induce @entity353 ; however, the mechanism underlying this phenomenon is unknown. The Mas receptor agonist @entity72115 is a metabolite of @entity4689 and of angiotensin II . As an agonist of Mas receptors, @entity72115 has beneficial cardiovascular and metabolic effects. EXPERIMENTAL APPROACH: We investigated the anti- @entity28 effects of transgenically overexpressed @entity72115 in @entity35 . We secondly examined whether @entity353 due to @entity9887 (8   mg  kg(-1)   d(-1) ) in diet-induced @entity28 Sprague Dawley (SD) @entity35 can be blocked when the animals were co-treated with the Mas receptor antagonist A779 (24 or 72    g  kg(-1)   d(-1) ). KEY RESULTS: In contrast to wild-type controls, transgenic @entity35 overexpressing angiotensin-(1-7) had 1.) diminished body weight when they were regularly fed with chow; 2.) were protected from developing @entity28 although they were fed with cafeteria diet (CD); 3.) showed a reduced energy intake that was mainly related to a lower CD intake; 5.) remained responsive to leptin despite chronic CD feeding; 6.) had a higher, strain-dependent energy expenditure, and 7.) were protected from developing insulin resistance despite CD feeding. @entity9887 -induced @entity353 in SD @entity35 was partially antagonized after a high, but not a low dose of A779. CONCLUSIONS AND IMPLICATIONS: Angiotensin-(1-7) regulated food intake and body weight and contributed to the @entity353 after AT1 receptor blockade. Angiotensin-(1-7)-like agonists may be drug candidates for treating @entity28 .
