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    Osteoblasts mediate the adverse effects of glucocorticoids on fuel metabolism.

    Glucocorticoid treatment is associated with weight gain, insulin resistance, and diabetes. Glucocorticoids also suppress osteoblast function, including the synthesis of osteocalcin, which is an osteoblast-specific peptide that is reported to be involved in normal murine fuel metabolism.  The authors found that  osteoblast-targeted disruption of glucocorticoid signaling significantly attenuated corticosterone-induced suppression of osteocalcin synthesis and the development of insulin resistance, glucose intolerance, and abnormal weight gain in mice. Nearly identical effects were observed in glucocorticoid-treated animals following heterotopic (hepatic) expression of both carboxylated and uncarboxylated osteocalcin through gene therapy.

    Brennan-Speranza TC, Henneicke H, Gasparini SJ, Blankenstein KI, Heinevetter U, Cogger VC, et al