Hormonal
Long-term glucocorticoid treatment causes insulin resistance, glucose intolerance, and abnormal weight gain by suppressing osteoblast function and osteocalcin synthesis; disrupting this skeletal signaling pathway prevents these metabolic adverse effects.
This research suggests that the metabolic side effects of long-term glucocorticoid use (like weight gain and insulin resistance) are partly driven by the suppression of bone-derived hormones (osteocalcin). While this is a mouse study, it implies that maintaining bone health or osteocalcin levels might mitigate metabolic risks in patients on steroids, though direct human interventions are not yet established.
Osteoblast-targeted disruption of glucocorticoid signaling significantly attenuated the suppression of osteocalcin synthesis and prevented the development of insulin resistance, glucose intolerance, and abnormal weight gain in corticosterone-treated mice.
Why this rating
High-quality controlled animal study with transgenic models and gene therapy, but results are not directly translatable to human clinical practice without further validation.
Source
Osteoblasts mediate the adverse effects of glucocorticoids on fuel metabolism
Tara C. Brennan‐Speranza et al. · Journal of Clinical Investigation · 2012
DOI 10.1172/jci63377
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