New insights into the biology of osteocalcin.

Autor: Zoch ML; Department of Orthopaedic Surgery, Johns Hopkins University School of Medicine, Baltimore, MD, USA., Clemens TL; Department of Orthopaedic Surgery, Johns Hopkins University School of Medicine, Baltimore, MD, USA; Baltimore Veterans Administration Medical Center, Baltimore, MD, USA., Riddle RC; Department of Orthopaedic Surgery, Johns Hopkins University School of Medicine, Baltimore, MD, USA; Baltimore Veterans Administration Medical Center, Baltimore, MD, USA. Electronic address: rriddle1@jhmi.edu.
Jazyk: angličtina
Zdroj: Bone [Bone] 2016 Jan; Vol. 82, pp. 42-9. Date of Electronic Publication: 2015 Jun 06.
DOI: 10.1016/j.bone.2015.05.046
Abstrakt: Osteocalcin is among the most abundant proteins in bone and is produced exclusively by osteoblasts. Initially believed to be an inhibitor of bone mineralization, recent studies suggest a broader role for osteocalcin that extends to the regulation of whole body metabolism, reproduction, and cognition. Circulating undercarboxylated osteocalcin, which is regulated by insulin, acts in a feed-forward loop to increase β-cell proliferation as well as insulin production and secretion, while skeletal muscle and adipose tissue respond to osteocalcin by increasing their sensitivity to insulin. Osteocalcin also acts in the brain to increase neurotransmitter production and in the testes to stimulate testosterone production. At least one putative receptor for osteocalcin, Gprc6a, is expressed by adipose, skeletal muscle, and the Leydig cells of the testes and appears to mediate osteocalcin's effects in these tissues. In this review, we summarize these new discoveries, which suggest that the ability of osteocalcin to function both locally in bone and as a hormone depends on a novel post-translational mechanism that alters osteocalcin's affinity for the bone matrix and bioavailability. This article is part of a Special Issue entitled Bone and diabetes.
(Copyright © 2015 Elsevier Inc. All rights reserved.)
Databáze: MEDLINE