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The osteoblast: Linking glucocorticoid-induced osteoporosis and hyperglycaemia? A post-hoc analysis of a randomised clinical trial

Glucocorticoids (GCs) induce osteoporosis predominantly by inhibiting osteoblast activity. We hypothesised that osteoblastic factors could also be linked to GC-induced adverse metabolic effects. We performed a post-hoc analysis of a randomised, placebo-controlled, double blind, dose-response interve...

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Bibliographic Details
Published in:Bone (New York, N.Y.) N.Y.), 2018-07, Vol.112, p.173-176
Main Authors: van Bommel, Erik J.M., de Jongh, Renate T., Brands, Myrte, Heijboer, Annemieke C., den Heijer, Martin, Serlie, Mireille J., van Raalte, Daniel H.
Format: Article
Language:English
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Summary:Glucocorticoids (GCs) induce osteoporosis predominantly by inhibiting osteoblast activity. We hypothesised that osteoblastic factors could also be linked to GC-induced adverse metabolic effects. We performed a post-hoc analysis of a randomised, placebo-controlled, double blind, dose-response intervention study involving 32 healthy males (age: 22 ± 3 years; BMI 22.4 ± 1.7 kg/m2) who were allocated to prednisolone (PRED) 7.5 mg once daily (n = 12), PRED 30 mg once daily (n = 12), or placebo (n = 8) for two weeks using block randomisation. Mean outcomes measures included osteocalcin, N-terminal propeptide of type 1 procollagen (P1NP) and their relation to glucose and lipid metabolism, measured by stable isotopes, before and at 2 weeks of treatment, in the fasted state and during a two-step hyperinsulinaemic clamp. Osteocalcin and P1NP concentrations were dose-dependently decreased by PRED treatment (p 
ISSN:8756-3282
1873-2763
DOI:10.1016/j.bone.2018.04.025