Regulation of Energy Metabolism by Bone-Derived Hormones

• Published in: Cold Spring Harbor perspectives in medicine Vol. 8; no. 6; p. a031666
• Main Authors: Mera, Paula, Ferron, Mathieu, Mosialou, Ioanna
• Format: Journal Article
• Language: English
• Published: United States Cold Spring Harbor Laboratory Press 01.06.2018
• Subjects: Animals; Bone and Bones - physiology; Energy Metabolism; Exercise; Glucose - physiology; Humans; Insulin - physiology; Lipocalin-2 - physiology; Osteocalcin - physiology; Receptor, Melanocortin, Type 4 - metabolism; Receptors, G-Protein-Coupled - metabolism; Signal Transduction
• ISSN: 2157-1422; 2472-5412
• DOI: 10.1101/cshperspect.a031666

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 β-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.