Journal
MOLECULAR AND CELLULAR ENDOCRINOLOGY
Volume 310, Issue 1-2, Pages 11-20Publisher
ELSEVIER IRELAND LTD
DOI: 10.1016/j.mce.2009.07.001
Keywords
Osteoblastogenesis; Osteoclastogenesis; Activin; Inhibin; Bone turnover
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Funding
- NIH [R01-DK54044, R21-DK74024, F31-DK079362]
- Porter Physiology Developmental Fellowship
- NASA Graduate Student Research Program
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There is both cellular and physiological evidence demonstrating that both Activins and Inhibins regulate osteoblastogenesis and osteoclastogenesis, and regulate bone mass in vivo. Although Activins and Inhibins were initially isolated from the gonad, Activins are also produced and stored in bone, whereas Inhibins exert their regulation on bone cell differentiation and metabolism via endocrine effects. The accumulating data provide evidence that reproductive hormones, distinct from classical sex steroids, are important regulators of bone mass and bone strength. Given the well described dominant antagonism of Inhibin over Activin, as well as over BMPs and TGF beta, the gonadally derived Inhibins are important regulators of locally produced osteotrophic factors. Thus, the cycling Inhibins in females and diurnal changes in Inhibin B in mates elicit temporal shifts in Inhibin levels (tone) that de-repress the pituitary. This fundamental action has the potential to de-repress locally stimulated changes in osteoblastogenesis and osteoclastogenesis, thereby altering bone metabolism. (C) 2009 Elsevier Ireland Ltd. All rights reserved.
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