Inactivation ofSocs3in the Hypothalamus Enhances the Hindbrain Response to Endogenous Satiety Signals via Oxytocin Signaling

• DOI: 10.1523/jneurosci.1669-12.2012
• Publication Date: 2012-11-28T17:43:04Z
• Authors: Valéry Matarazzo; Fabienne Schaller; Emmanuelle Nédélec; Alexandre Benani; Luc Pénicaud; Françoise Muscatelli; Emmanuel Moyse; Sylvian Bauer
• Keywords: Energy homeostasis; Hindbrain

Leptin is an adipocyte-derived hormone that controls energy balance by acting primarily in the CNS, but its action lost common forms of obesity due to central leptin resistance. One potential mechanism for such resistance increased hypothalamic expression Suppressor cytokine signaling 3 (Socs3), a feedback inhibitor Jak-Stat pathway prevents Stat3 activation. Ample studies have confirmed important role Socs3 and obesity. However, degree which participates regulation homeostasis nonobese conditions remains largely undetermined. In this study, using adult mice maintained under standard diet, we demonstrate deficiency mediobasal hypothalamus (MBH) reduces food intake, protects against body weight gain, limits adiposity, suggesting necessary normal maintenance. Mechanistically, MBH Socs3-deficient display hindbrain sensitivity endogenous, meal-related satiety signals, mediated oxytocin signaling. Thus, likely mediates effect on circuits caudal brainstem. This provides anatomical substrate meal size, more generally, how brain short-term intake as function energetic stores available organism maintain homeostasis. Any dysfunction could potentially lead overeating