Insulin, osteoblasts, and energy metabolism: Why bone counts calories

Research output: Contribution to journalComment/debatepeer-review

Abstract

Recent studies have demonstrated that insulin stimulates bone cells to produce and activate osteocalcin, an endocrine hormone that increases the efficiency of glucose metabolism through its actions on the pancreas and other peripheral tissues. In this issue of the JCI, Wei and colleagues directly explore the contribution of insulin signaling in osteoblasts to the disturbances in whole-body glucose metabolism associated with a high-fat diet. In mice fed a high-fat diet, increased uptake of saturated fatty acids by the osteoblast accelerates the ubiquitination and degradation of the insulin receptor. In this setting, impairments in osteoblast insulin signaling reduce serum levels of undercarboxylated osteocalcin, which in turn exacerbate insulin resistance in muscle and white adipose tissue. These findings underscore the importance of insulin-responsive skeletal cells as components of a newly appreciated endocrine network critical for regulating global energy homeostasis.

Original languageEnglish (US)
Pages (from-to)1465-1467
Number of pages3
JournalJournal of Clinical Investigation
Volume124
Issue number4
DOIs
StatePublished - Apr 1 2014

ASJC Scopus subject areas

  • Medicine(all)

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