Linked Life Data

7925099

Source:http://linkedlifedata.com/resource/pubmed/id/7925099

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
1994-10-24
pubmed:abstractText
Leydig cells are the major source of androgens in the male, and it is likely that these cells are also targets for androgen action. The role of androgen action in regulating the development of Leydig cell function has been determined using the testicular feminized (Tfm/Y) mouse, which lacks androgen receptors. In Tfm mice, the testes fail to descend at the normal time (25 days), and testicular descent was, therefore, surgically prevented in control (+/Y) animals. The activity of 3 beta-hydroxysteroid dehydrogenase increased during development from 5-40 days in control and Tfm mice, with no significant difference between the groups. In control animals, 17 alpha-hydroxylase activity was low from 5-25 days, at which time there was a 26-fold increase up to 40 days. In the Tfm group, 17 alpha-hydroxylase activity was 4-fold higher than that in controls on day 5, but showed no change in activity after 25 days and remained at neonatal levels up to 40 days. The activity of 17-ketosteroid reductase in the control animals showed a developmental pattern similar to that of 17 alpha-hydroxylase, with a marked increase in activity after 25 days. In the Tfm group, 17-ketosteroid reductase was normal on day 5, but failed to show any significant change thereafter and remained at neonatal levels on day 40. Serum LH levels in control animals increased from 5 days to a peak at 30 days. In Tfm mice, LH levels were significantly increased on days 20 and 40, but did not differ from controls on days 5, 25, and 30. In control +/Y animals, in which normal testicular descent was allowed to proceed at 25 days, the pattern of development was similar to that in the cryptorchid +/Y animals, although the increase in 17 alpha-hydroxylase activity at 30 and 40 days was significantly greater. The results show 1) that fetal Leydig cell steroidogenesis is enhanced in the absence of androgen receptors, but 2) that adult Leydig cells require receptor-mediated androgen activity around day 25 for normal functional development. In addition, 3) the lack of testicular descent at 25 days reduces the pubertal rise in 17 alpha-hydroxylase activity.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
0013-7227
pubmed:author
pubmed:issnType
Print
pubmed:volume
135
pubmed:geneSymbol
Tfm
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1372-7
pubmed:dateRevised
2009-9-29
pubmed:meshHeading
pubmed-meshheading:7925099-3-Hydroxysteroid Dehydrogenases, pubmed-meshheading:7925099-Androgens, pubmed-meshheading:7925099-Animals, pubmed-meshheading:7925099-Base Sequence, pubmed-meshheading:7925099-Cell Division, pubmed-meshheading:7925099-DNA, pubmed-meshheading:7925099-Drug Resistance, pubmed-meshheading:7925099-Leydig Cells, pubmed-meshheading:7925099-Luteinizing Hormone, pubmed-meshheading:7925099-Male, pubmed-meshheading:7925099-Mice, pubmed-meshheading:7925099-Mice, Inbred C3H, pubmed-meshheading:7925099-Mice, Mutant Strains, pubmed-meshheading:7925099-Molecular Sequence Data, pubmed-meshheading:7925099-Organ Size, pubmed-meshheading:7925099-RNA, Messenger, pubmed-meshheading:7925099-Receptors, Androgen, pubmed-meshheading:7925099-Sexual Maturation, pubmed-meshheading:7925099-Steroid 17-alpha-Hydroxylase, pubmed-meshheading:7925099-Testis, pubmed-meshheading:7925099-Time Factors
pubmed:year
1994
pubmed:articleTitle
Abnormal Leydig cell development at puberty in the androgen-resistant Tfm mouse.
pubmed:affiliation
Department of Veterinary Physiology, University of Glasgow Veterinary School, Scotland.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't