Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3 Pt 1
pubmed:dateCreated
1996-7-5
pubmed:abstractText
We investigated whether androgens, for which the ovaries are the major source in female rats, contribute to the stimulation of cancellous bone formation by ovarian hormones in female rats. Ovariectomized animals were administered 5alpha-dihydrotestosterone (DHT; 10 and 100 microgram/kg) by daily subcutaneous injection for 13 days, after which histomorphometric analysis was performed at the proximal tibial metaphysis. To prevent ovariectomy from stimulating bone turnover, and hence complicating the interpretation of changes in bone formation, animals were also given the resorption inhibitor 3-amino-1-hydroxypropylidene-1-bisphosphonate. We found that ovariectomy markedly suppressed cancellous bone formation, which was partially prevented by DHT (100 microgram/kg). To further address whether androgens contribute to the stimulation of bone formation by ovarian hormones, we treated intact and ovariectomized female rats with the androgen antagonist flutamide (15 mg/kg/day) for 28 days. Whereas flutamide had no effect in ovariectomized rats, it significantly reduced cancellous bone formation in intact animals. We conclude that, in the female rat, androgens contribute under physiological conditions to the stimulation of cancellous bone formation by ovarian hormones.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
0002-9513
pubmed:author
pubmed:issnType
Print
pubmed:volume
270
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
E407-12
pubmed:dateRevised
2010-8-25
pubmed:meshHeading
pubmed:year
1996
pubmed:articleTitle
Androgens contribute to the stimulation of cancellous bone formation by ovarian hormones in female rats.
pubmed:affiliation
Department of Histopathology, St. George's Hospital Medical School, London, United Kingdom.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't