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Cell Metab. 2013 Jun 4;17(6):901-15. doi: 10.1016/j.cmet.2013.04.009. Epub 2013 May 16.

Adiponectin regulates bone mass via opposite central and peripheral mechanisms through FoxO1.

Author information

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

Erratum in

  • Cell Metab. 2014 May 6;19(5):891. Guo, Edward X [corrected to Guo, X Edward].

Abstract

The synthesis of adiponectin, an adipokine with ill-defined functions in animals fed a normal diet, is enhanced by the osteoblast-derived hormone osteocalcin. Here we show that adiponectin signals back in osteoblasts to hamper their proliferation and favor their apoptosis, altogether decreasing bone mass and circulating osteocalcin levels. Adiponectin fulfills these functions, independently of its known receptors and signaling pathways, by decreasing FoxO1 activity in a PI3-kinase-dependent manner. Over time, however, these local effects are masked because adiponectin signals in neurons of the locus coeruleus, also through FoxO1, to decrease the sympathetic tone, thereby increasing bone mass and decreasing energy expenditure. This study reveals that adiponectin has the unusual ability to regulate the same function in two opposite manners depending on where it acts and that it opposes, partially, leptin's influence on the sympathetic nervous system. It also proposes that adiponectin regulation of bone mass occurs through a PI3-kinase-FoxO1 pathway.

PMID:
23684624
PMCID:
PMC3679303
DOI:
10.1016/j.cmet.2013.04.009
[Indexed for MEDLINE]
Free PMC Article

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