Modulation of XXXX metabolism by the renin-angiotensin- @entity1369 system.

@entity1 @entity1369 @entity101 @entity6 @entity63 @entity2178 @entity2270 @entity164 @entity209 @entity1720 @entity413
UNASSIGNED: The renin-angiotensin- @entity1369 system (RAAS) is an enzymatic cascade functioning in a paracrine and autocrine fashion. In animals and @entity1 , RAAS intrinsic to tissues modulates food intake, metabolic rate, @entity1720 , and insulin secretion. A large array of observations shows that dysregulation of RAAS in the @entity209 favors @entity164 2 @entity6 . Remarkably, angiotensin-converting enzyme inhibitors, suppressing the synthesis of @entity2178 ( @entity2178 ), and angiotensin receptor blockers, targeting the @entity2178 @entity164 1 receptor, prevent @entity6 in @entity1 with @entity101 or @entity63 . These drugs interrupt the negative feedback loop of @entity2178 on the RAAS cascade, which results in increased production of angiotensins. In addition, they change the tissue expression of RAAS components. Therefore, the concept of a dual @entity2270 of RAAS regarding @entity413 homeostasis has emerged. The RAAS deleterious @entity2270 increases the production of inflammatory cytokines and raises oxidative stress, exacerbating the insulin resistance and decreasing insulin secretion. The @entity2270 promotes adipogenesis, blocks the production of inflammatory cytokines, and lowers oxidative stress, thereby improving insulin sensitivity and secretion. Currently, drugs targeting RAAS are not given for the purpose of preventing @entity6 in @entity1 . However, we anticipate that in the near future the discovery of novel means to modulate the RAAS @entity2270 will result in a decisive therapeutic breakthrough.
