Abstract
Evidence indicates that activation of the angiotensin II type 1 receptor (AT1R) acutely decreases insulin secretion in animals and humans (1–3), mediated at least partially by reductions in islet blood flow and proinsulin biosynthesis (1,2). In contrast, AT1R blockade increased insulin secretion by 40–60% in Zucker diabetic fatty (ZDF) rats (4) and in obese db/db mice (5), thereby delaying the otherwise premature onset of diabetes in the latter animal model. If this were the case in humans, it would provide an explanation for the finding that AT1R antagonist treatment reduces the incidence of type 2 diabetes by ∼25% in high-risk individuals in clinical trials despite no improvement in insulin sensitivity in most …
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