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Effects of eldecalcitol on bone and skeletal muscles in glucocorticoid treated rats

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Glucocorticoid causes secondary osteoporosis and myopathy, characterized by type II muscle fiber atrophy. We examined whether a new vitamin D3 analog, eldecalcitol, could inhibit glucocorticoid-induced osteopenia or myopathy in rats and determined the effects of prednisolone (PSL) and/or eldecalcitol on muscle-related gene expression. Six-month-old female Wistar rats were randomized into four groups: PSL group (10 mg/kg PSL); E group (0.05 µg/kg eldecalcitol); PSL + E group; and control group. PSL, eldecalcitol, and vehicles were administered daily for 2 or 4 weeks. Right calf muscle strength, muscle fatigue, cross-sectional areas (CSAs) of left tibialis anterior muscle fibers, and bone mineral density (BMD) were measured following administration. Pax7, MyoD, and myogenin mRNA levels in gastrocnemius muscles were also determined. The PSL + E group muscle strength was significantly higher than that of the PSL group (p < 0.05) after 4 but not 2 weeks. There was no significant difference in muscle fatigue between the groups at 2 or 4 weeks. The CSAs of type II muscle fibers were significantly larger in the E group and PSL + E group than the PSL group at 4 weeks (p = 0.0093, p = 0.0443, respectively). Eldecalcitol treatment for 4 weeks maintained the same BMD as the PSL + E group. After 2 but not 4 weeks, eldecalcitol treatment significantly increased Pax7 and myogenin mRNA expression in gastrocnemius muscle, while PSL also stimulated myogenin expression. Eldecalcitol appears to increase muscle volume and protect against femur BMD loss in PSL-administered rats. It may also stimulate myoblast differentiation into early myotubes.


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