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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
5594
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pubmed:dateCreated |
2002-10-25
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pubmed:abstractText |
We show that sex steroids protect the adult murine skeleton through a mechanism that is distinct from that used to preserve the mass and function of reproductive organs. The classical genotropic actions of sex steroid receptors are dispensable for their bone protective effects, but essential for their effects on reproductive tissues. A synthetic ligand (4-estren-3alpha,17beta-diol) that reproduces the nongenotropic effects of sex steroids, without affecting classical transcription, increases bone mass and strength in ovariectomized females above the level of the estrogen-replete state and is at least as effective as dihydrotestosterone in orchidectomized males, without affecting reproductive organs. Such ligands merit investigation as potential therapeutic alternatives to hormone replacement for osteoporosis in both women and men [corrected].
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pubmed:grant |
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pubmed:commentsCorrections |
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:month |
Oct
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pubmed:issn |
1095-9203
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pubmed:author |
pubmed-author:AliA AAA,
pubmed-author:BöJJ,
pubmed-author:BellidoTT,
pubmed-author:ChenJ RJR,
pubmed-author:EbertRR,
pubmed-author:HaqAA,
pubmed-author:JilkaR LRL,
pubmed-author:KousteniSS,
pubmed-author:MancinoA TAT,
pubmed-author:ManolagasS CSC,
pubmed-author:O'BrienC ACA,
pubmed-author:ParfittA MAM,
pubmed-author:PlotkinLL,
pubmed-author:PowersC CCC,
pubmed-author:StewartS ASA,
pubmed-author:VertinoA MAM,
pubmed-author:WeinsteinR SRS,
pubmed-author:WenYY
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pubmed:issnType |
Electronic
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pubmed:day |
25
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pubmed:volume |
298
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
843-6
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pubmed:dateRevised |
2007-11-14
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pubmed:meshHeading |
pubmed-meshheading:12399595-Animals,
pubmed-meshheading:12399595-Apoptosis,
pubmed-meshheading:12399595-Body Weight,
pubmed-meshheading:12399595-Bone Density,
pubmed-meshheading:12399595-Bone and Bones,
pubmed-meshheading:12399595-Breast Neoplasms,
pubmed-meshheading:12399595-Cell Division,
pubmed-meshheading:12399595-Cells, Cultured,
pubmed-meshheading:12399595-Compressive Strength,
pubmed-meshheading:12399595-Dihydrotestosterone,
pubmed-meshheading:12399595-Estradiol,
pubmed-meshheading:12399595-Estrenes,
pubmed-meshheading:12399595-Female,
pubmed-meshheading:12399595-Humans,
pubmed-meshheading:12399595-Male,
pubmed-meshheading:12399595-Mice,
pubmed-meshheading:12399595-Orchiectomy,
pubmed-meshheading:12399595-Organ Size,
pubmed-meshheading:12399595-Osteoblasts,
pubmed-meshheading:12399595-Osteocalcin,
pubmed-meshheading:12399595-Osteoclasts,
pubmed-meshheading:12399595-Osteogenesis,
pubmed-meshheading:12399595-Osteoporosis,
pubmed-meshheading:12399595-Ovariectomy,
pubmed-meshheading:12399595-Pyrazoles,
pubmed-meshheading:12399595-Receptors, Estrogen,
pubmed-meshheading:12399595-Seminal Vesicles,
pubmed-meshheading:12399595-Transcription, Genetic,
pubmed-meshheading:12399595-Tumor Cells, Cultured,
pubmed-meshheading:12399595-Uterus
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pubmed:year |
2002
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pubmed:articleTitle |
Reversal of bone loss in mice by nongenotropic signaling of sex steroids.
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pubmed:affiliation |
Division of Endocrinology and Metabolism, Department of Internal Medicine, and Center for Osteoporosis and Metabolic Bone Diseases, University of Arkansas for Medical Sciences, Little Rock, AR 72205, USA.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, U.S. Gov't, Non-P.H.S.,
Research Support, Non-U.S. Gov't
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