Key result
Intracerebroventricularly administered angiotensin II and III dose-dependently suppressed food intake in mice through AT2 receptor and subsequent EP4 receptor activation.
Centrally administered angiotensin II and III suppress food intake via a novel pathway involving the AT2 receptor and subsequent EP4 receptor activation.
May implicate central AT2 receptors in appetite control; leaves open translation to human therapies.
Intracerebroventricularly administered angiotensin (Ang) II and III dose-dependently suppressed food intake in mice and their anorexigenic activities were inhibited by AT(2) receptor-selective antagonist. Ang II did not suppress food intake in AT(2) receptor-knockout mice, while it did significantly in wild-type and AT(1) receptor-knockout mice. The suppression of food intake in AT(1) receptor-knockout mice was smaller than that in wild-type. The anorexigenic activities of Ang II and III were also blocked by a selective antagonist for prostaglandin EP(4) receptor. Taken together, centrally administered Ang II and III may decrease food intake through AT(2) receptor with partial involvement of AT(1) receptor, followed by EP(4) receptor activation, which is a novel pathway regulating food intake.
No takes yet. Share an insight, caveat, or question.
Ohinata et al. (2008) studied this question. Intracerebroventricularly administered angiotensin (Ang) II and III vs. Receptor antagonists and knockout models was evaluated on Food intake. Intracerebroventricularly administered angiotensin II and III dose-dependently suppressed food intake in mice through AT2 receptor and subsequent EP4 receptor activation.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: