Testosterone supplementation, glucocorticoid milieu and bone homeostasis in the ageing male.
2017
Tip dokumenta:
Članak u časopisu (Objavljena verzija)
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© 2017 Société Française de Pharmacologie et de Thérapeutique
Metapodaci
Prikaz svih podataka o dokumentuApstrakt:
Male ageing is entwined with a continuous fall in free testosterone levels, which contributes to the pathogenesis of bone loss. Glucocorticoid excess, either dependent on the ageing process or iatrogenically induced, was found to additionally impair the bone structure and metabolism. Cautious testosterone supplementation in this respect may positively affect the glucocorticoid milieu and bone homeostasis, while testosterone-induced changes in the glucocorticoid output could serve as a determinant of bone-related therapeutic outcome. Namely, bone mineral content/density, the parameters of trabecular bone structure as well as bone strength are enhanced, serum calcitonin levels tend to increase, while serum osteocalcin, serum parathyroid hormone and urinary calcium decrease, all upon testosterone administration to the ageing male. In parallel, testosterone application decreases glucocorticoid secretion in the animal models of male ageing, while clinical data in this field are still inconsistent. Importantly, a physiological link exists between testosterone-induced changes in glucocorticoid levels and the tendency of bone status improvement in the ageing male. We believe that the assessment of circulating adrenocorticotropic hormone concentrations together with glucocorticoid levels, reflecting the hypothalamic-pituitary-adrenal axis feedback loop operativeness during testosterone supplementation, represents a well-balanced bone-related therapeutic update.
Ključne reči:
Ageing; Bone; Glucocorticoid; Male; Testosterone supplementationIzvor:
Fundamental & clinical pharmacology, 2017, 31, 4, 372-382Finansiranje / projekti:
- Odgovor neuroendokrinog sistema pacova na odabrane biljne ekstrakte, fitoestrogene, steroidne i peptidne hormone (RS-MESTD-Basic Research (BR or ON)-173009)
DOI: 10.1111/fcp.12277
ISSN: 0767-3981
PubMed: 28186359
WoS: 000404885500001
Scopus: 2-s2.0-85014003321
URI
http://doi.wiley.com/10.1111/fcp.12277http://www.ncbi.nlm.nih.gov/pubmed/28186359
https://radar.ibiss.bg.ac.rs/handle/123456789/2607