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by Leigh MacMillan | Posted on Tuesday, Jul. 3, 2012 — 8:37 AM
Defects in the melanocortin-4 receptor cause a genetic obesity syndrome in humans and have implicated melanocortin brain circuitry in regulating long-term energy balance. The role of the melanocortin-3 receptor (MC3-R) in modulating energy balance is less clear. Deletion of the MC3-R gene in mice causes mild obesity, without hyperphagia (abnormally increased appetite) or hypometabolism.
Roger Cone, Joe C. Davis Chair in Biomedical Science, and colleagues have now characterized the mechanistic changes underlying this mild obesity syndrome. They report in the June 5 Proceedings of the National Academy of Sciences that mice missing MC3-R have defective responses to fasting, such as blunted mobilization of fatty acids from adipose tissue and reduced activation of the central hypothalamic-pituitary-adrenal signaling axis. These defects alter nutrient distribution and increase fat tissue. The researchers also showed that MC3-R deletion resulted in a Cushing-like syndrome with elevated levels of corticosteroids.
The findings suggest a specific role for MC3-R-containing brain circuits in communicating nutritional status and in regulating nutrient distribution in response to fasting.
This research was supported by a grant from the National Institute of Diabetes and Digestive and Kidney Diseases (DK078850) of the National Institutes of Health and by the VA Medical Research Service.
Leigh MacMillan, (615) 322-4747
Health and Medicine, Reporter, Research Aliquots, appetite, brain, fasting, journal publication, melanocortin, metabolism, molecular physiology and biophysics, NIDDK, NIH, nutrition, obesity, PNAS, Reporter June 22 2012, Roger Cone, VA Medical Research Service
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