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.
journal_name
Celljournal_title
Cellauthors
Ferron M,Wei J,Yoshizawa T,Del Fattore A,DePinho RA,Teti A,Ducy P,Karsenty Gdoi
10.1016/j.cell.2010.06.003subject
Has Abstractpub_date
2010-07-23 00:00:00pages
296-308issue
2eissn
0092-8674issn
1097-4172pii
S0092-8674(10)00621-5journal_volume
142pub_type
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