Further information

Regulation of Homeostatic Boundary Control and Rheostasis by the Melanocortin-3 Receptor

9706 1493124765

Talk by Professor Roger Cone, University of Michigan, USA

  • Date: May 15, 2017
  • Time: 14:00 - 15:00
  • Speaker: Roger D. Cone, Ph.D.
  • Mary Sue Coleman Director, Life Sciences Institute, Professor of Molecular and Integrative Physiology, University of Michigan, USA
  • Location: MPI for Metabolism Research, Gleueler Strasse 50, 50931 Köln
  • Room: Seminar room 1
  • Host: Dr. Rachel Lippert
  • Contact: rachel.lippert@sf.mpg.de
The MC4R regulates energy homeostasis, and haploinsufficiency produces hyperphagia, hypometabolism, and early onset obesity. In contrast, homozygous deletion of the MC3R does not cause hyperphagia or hypometabolism under normal conditions, producing a mild, late-onset obesity. However, the MC3R plays a critical role in regulating energy homeostasis in response to external and internal nutritional challenges. First, the MC3R regulates energy stores in response to fasting and chronic food restriction. Additionally, there are multiple roles for MC3R in regulation of energy homeostasis in response to reproductive state. MC3R KO mice exhibit defective pregnancy-induced hyperphagia and defective control of energy stores in response to ovariectomy. Thus, MC3R deletion results in defective homeostatic boundary control and rheostasis. Additional data demonstrate a molecular mechanism by which MC3R regulates homeostatic boundary control: MC3R on AgRP neurons acts presynaptically to provide autoregulatory feedback onto MC4R PVN neurons.
 
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