BGLAP and Insulin resistance: Moreover, more recent studies in different mice models demonstrated that osteoblast-targeted disruption of glucocorticoid signaling (due to transgenic overexpression of the glucocorticoid-inactivating enzyme 11β-hydroxysteroid dehydrogenase type 2) significantly attenuated the suppression of osteocalcin synthesis and prevented the development of insulin resistance, glucose intolerance, and abnormal weight gain induced by corticosterone treatment [29].