Journal
COLD SPRING HARBOR PERSPECTIVES IN MEDICINE
Volume 8, Issue 6, Pages -Publisher
COLD SPRING HARBOR LAB PRESS, PUBLICATIONS DEPT
DOI: 10.1101/cshperspect.a031666
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Funding
- Canada Research Chair program
- Canadian Institutes of Health Research [MOP-133652]
- Natural Sciences and Engineering Research Council of Canada
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Like many other organs, bone can act as an endocrine organ through the secretion of bone-specific hormones or osteokines. At least two osteokines are implicated in the control of glucose and energy metabolism: osteocalcin (OCN) and lipocalin-2 (LCN2). OCN stimulates the production and secretion of insulin by the pancreatic n-cells, but also favors adaptation to exercise by stimulating glucose and fatty acid (FA) utilization by the muscle. Both of these OCN functions are mediated by the G-protein-coupled receptor GPRC6A. In contrast, LCN2 influences energy metabolism by activating appetite-suppressing signaling in the brain. This action of LCN2 occurs through its binding to the melanocortin 4 receptor (MC4R) in the paraventricular nucleus of the hypothalamus (PVN) and ventromedial neurons of the hypothalamus.
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