Kate L. J. Ellacott

TL;DR: It is shown that mouse brainstem NTS POMC neurons are activated by cholecystokinin and feeding-induced satiety and that activation of the neuronal melanocortin-4 receptor (MC4-R) is required for CCK-induced suppression of feeding; the melanoc Cortin system thus provides a potential substrate for integration of long-term adipostatic and short-term satiety signals.

TL;DR: Evidence for the existence of a similar network of neurons in the NTS and a model by which this information from the ARC and NTS centers may be integrated directly or via adipostatic centers such as the paraventricular nucleus of the hypothalamus (PVH).

TL;DR: This review will focus on the benefits and caveats of the most common mouse models of MetS, which have been used for decades to determine the pathophysiological basis for MetS and how MetS increases the risk for other diseases.

TL;DR: It is demonstrated that, like cholecystokinin, PYY(3-36) dose-dependently inhibits food intake by approximately 20-45% over a 3- to 4-h period post ip administration, with no effect on 12-h food intake, and PYY-induced satiety is atypical, because it does not produce detectable activation of brainstem satiety centers and is not dependent on MC4-R signaling.

TL;DR: This document represents the current consensus view of investigators from the National Institutes of Health-funded Mouse Metabolic Phenotyping Centers (MMPCs) and can be applied to most other animal models.