Format

Send to:

Choose Destination
See comment in PubMed Commons below
Cell. 2010 Jul 23;142(2):296-308. doi: 10.1016/j.cell.2010.06.003.

Insulin signaling in osteoblasts integrates bone remodeling and energy metabolism.

Author information

  • 1Department of Genetics and Development, College of Physicians and Surgeons, Columbia University, New York, NY 10032, USA.

Abstract

The broad expression of the insulin receptor suggests that the spectrum of insulin function has not been fully described. A cell type expressing this receptor is the osteoblast, a bone-specific cell favoring glucose metabolism through a hormone, osteocalcin, that becomes active once uncarboxylated. We show here that insulin signaling in osteoblasts is necessary for whole-body glucose homeostasis because it increases osteocalcin activity. To achieve this function insulin signaling in osteoblasts takes advantage of the regulation of osteoclastic bone resorption exerted by osteoblasts. Indeed, since bone resorption occurs at a pH acidic enough to decarboxylate proteins, osteoclasts determine the carboxylation status and function of osteocalcin. Accordingly, increasing or decreasing insulin signaling in osteoblasts promotes or hampers glucose metabolism in a bone resorption-dependent manner in mice and humans. Hence, in a feed-forward loop, insulin signals in osteoblasts activate a hormone, osteocalcin, that promotes glucose metabolism.

Copyright 2010 Elsevier Inc. All rights reserved.

PMID:
20655470
[PubMed - indexed for MEDLINE]
PMCID:
PMC2910411
Free PMC Article
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for PubMed Central
    Loading ...
    Write to the Help Desk