西亚试剂：Endocrine Regulation of Energy Metabolism by the Skeleton

Endocrine Regulation of Energy Metabolism by the Skeleton

Na Kyung Lee,1 Hideaki Sowa,1 Eiichi Hinoi,1 Mathieu Ferron,1 Jong Deok Ahn,3 Cyrille Confavreux,1 Romain Dacquin,4 Patrick J. Mee,5 Marc D. McKee,6 Dae Young Jung,7 Zhiyou Zhang,7 Jason K. Kim,7 Franck Mauvais-Jarvis,8 Patricia Ducy,2 and Gerard Karsenty1,

1 Department of Genetics & Development, College of Physicians and Surgeons, Columbia University, New York, NY 10032, USA
2 Department of Pathology, College of Physicians and Surgeons, Columbia University, New York, NY 10032, USA
3 CHO-A Biotechnology Research Institute, CHO-A Pharm. Co., Seoul 143-701, Korea
4 Ecole Normale Supérieure de Lyon, UMR5161, Laboratoire d'Endocrinologie Moléculaire et Différenciation Hématopoïétique et Osseuse, 69364 Lyon, France
5 Centre for Stem Cell Research, University of Cambridge, Cambridge CB2 1TN, United Kingdom
6 Faculty of Dentistry, and Department of Anatomy and Cell Biology, McGill University, Montreal, QC, Canada H3A 2B2
7 Department of Cellular & Molecular Physiology, Penn State Medical Center, Hershey, PA 17033
8 Department of Medicine, Northwestern University School of Medicine, Chicago, IL 60611, USA

Corresponding author
Gerard Karsenty
The regulation of bone remodeling by an adipocyte-derived hormone implies that bone may exert a feedback control of energy homeostasis. To test this hypothesis we looked for genes expressed in osteoblasts, encoding signaling molecules and affecting energy metabolism. We show here that mice lacking the protein tyrosine phosphatase OST-PTP are hypoglycemic and are protected from obesity and glucose intolerance because of an increase in β-cell proliferation, insulin secretion, and insulin sensitivity. In contrast, mice lacking the osteoblast-secreted molecule osteocalcin display decreased β-cell proliferation, glucose intolerance, and insulin resistance. Removing one Osteocalcin allele from OST-PTP-deficient mice corrects their metabolic phenotype. Ex vivo, osteocalcin can stimulate CyclinD1 and Insulin expression in β-cells and Adiponectin, an insulin-sensitizing adipokine, in adipocytes; in vivo osteocalcin can improve glucose tolerance. By revealing that the skeleton exerts an endocrine regulation of sugar homeostasis this study expands the biological importance of this organ and our understanding of energy metabolism.

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