Key points are not available for this paper at this time.
Design
Review
Adipose RAS mechanisms may guide future RAS inhibitor use in obese patients; leaves open clinical validation of targeted interventions.
Summary Angiotensin II (Ang II), acting on the AT 1 and AT 2 receptors in mammalian cells, is the vasoactive component of the renin‐angiotensin system (RAS). Several components of the RAS have been demonstrated in different tissues, including adipose tissue. Although the effects of Ang II on metabolism have not been studied widely, it is intriguing to assume that components of the RAS produced by adipocytes may play an autocrine, a paracrine and/or an endocrine role in the pathophysiology of obesity and provide a potential pathway through which obesity leads to hypertension and type 2 diabetes mellitus. In the first part of this review, we will describe the production of Ang II, the different receptors through which Ang II exerts its effects and summarize the concomitant intracellular signalling cascades. Thereafter, potential Ang II‐induced mechanisms, which may be associated with obesity and obesity‐related disorders, will be considered. Finally, we will focus on the different pharmaceutical agents that interfere with the RAS and highlight the possible implications of these drugs in the treatment of obesity‐related disorders.
No takes yet. Share an insight, caveat, or question.
Goossens et al. (2003) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: