ISSN 1470-3947 (print) | ISSN 1479-6848 (online)

Endocrine Abstracts (2008) 16 EJE1

Sex steroids in the regulation of bone metabolism in men

Claes Ohlsson

Division of Endocrinology, Department of Internal Medicine, Sahlgrenska University Hospital, Goteborg, Sweden

Osteoporosis-related fractures constitute a major health concern not only in women but also in men. The relative contribution of estrogens and androgens for the male skeleton remains unclear. Most epidemiological studies demonstrate that serum estradiol is a stronger predictor of bone mineral density than serum testosterone. However, conflicting results have been presented regarding the impact of serum sex steroids for fracture risk in men, probably because previous studies have been underpowered and have analyzed the serum sex steroid levels using immunoassay-based techniques with a questionable specificity at lower concentrations. We recently showed that elderly men with low serum estradiol have an increased risk of fractures in the large population-based MrOS Sweden study, with serum sex steroids analyzed by the specific gas chromatography–mass spectrometry technique. In contrast, serum testosterone was not an independent predictor of fracture risk.

There are two main sources of sex steroids in elderly men, the testicles and the adrenals. Interestingly, we found that low serum DHEA was related to fracture risk independently of serum sex steroids in the MrOS Sweden study, indicating that adrenal-derived DHEA, which is locally converted to estradiol and/or testosterone, has an impact on fracture risk.

Experiments using mice with inactivated sex steroid receptors demonstrated that both activation of the estrogen receptor (ER)α and activation of the androgen receptor (AR) result in a stimulatory effect on the cancellous bone mass in males. ERβ was of no importance for the skeleton in male mice while it modulated the ERα-action on cancellous bone in females. In vitro studies demonstrated that the G-protein coupled receptor GPR30 is a functional ER. Our recent in vivo analyses of GPR30-inactivated mice revealed no function of GPR30 for cancellous bone mass but it is involved in estrogen-mediated insulin secretion and modulates longitudinal bone growth.

Article tools

My recent searches

No recent searches.

My recently viewed abstracts