Linked Life Data

12865302

Source:http://linkedlifedata.com/resource/pubmed/id/12865302

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
8
pubmed:dateCreated
2003-7-16
pubmed:abstractText
Adult Leydig cell steroidogenesis is dependent on LH but fetal Leydig cells can function independently of gonadotropin stimulation. To identify factors that may be involved in regulation of fetal Leydig cells expressed sequence tag libraries from fetal and adult testes were compared, and fetal-specific genes identified. The ACTH receptor [melanocortin type 2 receptor (Mc2r)] was identified within this fetal-specific group. Subsequent real-time PCR studies confirmed that Mc2r was expressed in the fetal testis at 100-fold higher levels than in the adult testis. Incubation of fetal or neonatal testes with ACTH in vitro stimulated testosterone production more than 10-fold, although ACTH had no effect on testes from animals aged 20 d or older. The steroidogenic response of fetal and neonatal testes to a maximally stimulating dose of human chorionic gonadotropin was similar to the response shown to ACTH. The ED(50) for ACTH, measured in isolated fetal and neonatal testicular cells, was 5 x 10(-10) M and the lowest dose of ACTH eliciting a response was 2 x 10(-11) M. Circulating ACTH levels in fetal mice were around 8 x 10(-11) M. Neither alpha-MSH nor gamma-MSH had any effect on androgen production in vitro at any age. Fetal testosterone levels were normal in mice that lack circulating ACTH (proopiomelanocortin-null) indicating that ACTH is not essential for fetal Leydig cell function. Results show that both LH and ACTH can regulate testicular steroidogenesis during fetal development in the mouse and suggest that fetal Leydig cells, but not adult Leydig cells, are sensitive to ACTH stimulation.
pubmed:commentsCorrections
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
0013-7227
pubmed:author
pubmed:issnType
Print
pubmed:volume
144
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
3279-84
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:12865302-Adrenocorticotropic Hormone, pubmed-meshheading:12865302-Animals, pubmed-meshheading:12865302-Animals, Newborn, pubmed-meshheading:12865302-Chorionic Gonadotropin, pubmed-meshheading:12865302-Leydig Cells, pubmed-meshheading:12865302-Luteinizing Hormone, pubmed-meshheading:12865302-Male, pubmed-meshheading:12865302-Mice, pubmed-meshheading:12865302-Mice, Inbred C3H, pubmed-meshheading:12865302-Mice, Knockout, pubmed-meshheading:12865302-Polymerase Chain Reaction, pubmed-meshheading:12865302-Pro-Opiomelanocortin, pubmed-meshheading:12865302-Receptor, Melanocortin, Type 2, pubmed-meshheading:12865302-Receptors, Corticotropin, pubmed-meshheading:12865302-Testis, pubmed-meshheading:12865302-Testosterone, pubmed-meshheading:12865302-alpha-MSH, pubmed-meshheading:12865302-gamma-MSH
pubmed:year
2003
pubmed:articleTitle
Adrenocorticotropic hormone directly stimulates testosterone production by the fetal and neonatal mouse testis.
pubmed:affiliation
Institute of Comparative Medicine, University of Glasgow Veterinary School, Glasgow, Scotland G61 1QH, United Kingdom. p.j.o'shaughnessy@vet.gla.ac.uk
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't