Insulin signaling in osteoblasts integrates bone remodeling and energy metabolism
By Mathieu Ferron, Jianwen Wei, T. Yoshizawa, A. D. Fattore, R. DePinho, A. Teti, P. Ducy, G. Karsenty. Cell, 2010
1,123 citations recorded by the source corpus.
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 acid 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 to activate a hormone, osteocalcin, that promotes glucose metabolism.
Subfields: Molecular Biology, Oncology
View Paper: https://www.semanticscholar.org/paper/4f1f243ee9bf2475c2f96f0c214984751361e46f
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Citations in the corpus
- Building strong bones: molecular regulation of the osteoblast lineage (2011, background): “In addition, recent studies in mice have suggested unexpected roles for osteoblast lineage cells in regulating glucose metabolis”
- Endocrine regulation of male fertility by the skeleton. (2011, neutral): “A second gene expressed in osteoblasts, Esp, inhibits endocrine functions of osteocalcin by favoring, through an indirect mechanism, its carboxylation (Ferron et al., 2010; Fulzele et al., 2010).”