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- Lindberg, Marie K, 1975, et al.
(författare)
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Two different pathways for the maintenance of trabecular bone in adult male mice.
- 2002
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Ingår i: Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research. - : Wiley. - 0884-0431. ; 17:4, s. 555-62
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Tidskriftsartikel (refereegranskat)abstract
- Androgens may regulate the male skeleton either directly via activation of the androgen receptor (AR) or indirectly via aromatization of androgens into estrogen and, thereafter, via activation of estrogen receptors (ERs). There are two known estrogen receptors, ER-alpha and ER-beta. The aim of this study was to investigate the relative roles of ER-alpha, ER-beta, and AR in the maintenance of trabecular bone in male mice. Seven-month-old male mice, lacking ER-alpha (ERKO), ER-beta (BERKO), or both receptors (DERKO), were orchidectomized (orx) and treated for 3 weeks with 0.7 microg/mouse per day of 17beta-estradiol or vehicle. No reduction in trabecular bone mineral density (BMD) was seen in ERKO, BERKO, or DERKO mice before orx, showing that neither ER-a nor ER-beta is required for the maintenance of a normal trabecular BMD in male mice. After orx, there was a pronounced decrease in trabecular BMD, similar for all groups, resulting in equal levels of trabecular BMD in all genotypes. This reduction was reversed completely in wild-type (WT) and BERKO mice treated with estrogen, and no significant effect of estrogen was found in ERKO or DERKO mice. In summary, the trabecular bone is preserved both by a testicular factor, presumably testosterone acting via AR and by an estrogen-induced activation of ER-alpha. These results indicate that AR and ER-alpha are redundant in the maintenance of the trabecular bone in male mice. In contrast, ER-beta is of no importance for the regulation of trabecular bone in male mice.
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- Wang, Qingju, et al.
(författare)
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Differential effects of sex hormones on peri- and endocortical bone surfaces in pubertal girls.
- 2006
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Ingår i: The Journal of clinical endocrinology and metabolism. - : The Endocrine Society. - 0021-972X .- 1945-7197. ; 91:1, s. 277-82
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Tidskriftsartikel (refereegranskat)abstract
- CONTEXT: The role of sex steroids in bone growth in pubertal girls is not yet clear. Bone biomarkers are indicators of bone metabolic activity, but their value in predicting bone quality has not been studied in growing girls. OBJECTIVE: This study examines the association of sex hormones and bone markers with bone geometry and density in pubertal girls. DESIGN: The study was designed as a 2-yr longitudinal study in pubertal girls. Measurements were performed at baseline and at 1- and 2-yr follow-ups. SETTING: The study was conducted in a university laboratory. PARTICIPANTS: A total of 258 10- to 13-yr-old healthy girls at the baseline participated. METHODS: Peripheral quantitative computed tomography was used to scan the left tibial shaft. Serum 17beta-estradiol (E2), testosterone (T), SHBG, osteocalcin (OC), bone-specific alkaline phosphatase, and tartrate-resistant acid phosphatase isoform 5b were assessed. Data were analyzed using hierarchical linear models with random effect. RESULTS: E2 was a positive predictor for total bone mineral density (BMD), cortical thickness, and a negative predictor for endocortical circumference but had no predictive value for total bone cross-sectional area or periosteal circumference. T was a positive predictor for total cross-sectional area and periosteal circumference as well as endocortical circumference, and a negative predictor for total BMD. OC was negatively correlated with cortical BMD (R2 = 0.325; P < 0.001). CONCLUSIONS: In pubertal girls, E2 and T have different influences on bone properties at the long bone shaft. The results suggest that, at the endocortical surface, E2 inhibits bone resorption during rapid growth, and later, after menarche, acts at higher concentrations to promote bone formation. At the periosteal surface, T promotes bone formation, whereas E2 does not affect it. In addition, OC might be used as a predictor of cortical BMD.
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