Journal
CELL
Volume 125, Issue 2, Pages 247-260Publisher
CELL PRESS
DOI: 10.1016/j.cell.2006.01.051
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Funding
- NIAMS NIH HHS [AR47700, AR41010, R01 AR041210] Funding Source: Medline
- NIA NIH HHS [AG23176, AG12951, AG14907] Funding Source: Medline
- NIDDK NIH HHS [DK70526] Funding Source: Medline
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Postmenopausal osteoporosis, a global public health problem, has for decades been attributed solely to declining estrogen levels. Although FSH levels rise sharply in parallel, a direct effect of FSH on the skeleton has never been explored. We show that FSH is required for hypogonadal bone loss. Neither FSH beta nor FSH receptor (FSHR) null mice have bone loss despite severe hypogonadism. Bone mass is increased and osteoclastic resorption is decreased in haploin-sufficient FSHD+/- mice with normal ovarian function, suggesting that the skeletal action of FSH is estrogen independent. Osteoclasts and their precursors possess G(i2 alpha)-COupled FSHRs that activate MEK/Erk, NF-kappa B, and Akt to result in enhanced osteoclast formation and function. We suggest that high circulating FSH causes hypogonadal bone loss.
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