Document Detail


Growth hormone (GH) response to GH-releasing hormone by perifused pituitary cells from male, female, and testicular feminized rats.
MedLine Citation:
PMID:  2491809     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
To determine whether a normal complement of androgen receptors is required to permit full expression of sex-related differences in pituitary GH secretion, we compared the GHRH-stimulated GH secretory responses of continuously perifused anterior pituitary cells from normal male, normal female, and androgen-resistant testicular feminized (Tfm) rats. In each experimental replicate, acutely dispersed pituitary cells were exposed to GHRH (0.03-100 nM) administered as 2.5-min pulses in random order at 30-min intervals. The eluate was collected in 5-min fractions for GH determination by RIA. Basal unstimulated secretion of GH by cells from male rats was greater than that by cells from female (P = 0.007) and Tfm (P = 0.03) rats; basal secretion by the other two groups was similar (P = 0.55). Linear concentration-response relationships between GHRH and GH release were defined for cells from male (P = 0.0002), female (P = 0.0001), and Tfm (P = 0.0002) rats. Overall GHRH-stimulated GH secretion by cells from male rats was greater (P less than 0.0001) than that by cells from female rats. Overall secretion by cells from Tfm rats was less (P less than 0.001) than that by cells from male rats but greater (P less than 0.001) than that by cells from female rats. For all experimental groups, body weight was strongly correlated with both basal (r2 = 0.42; P = 0.001) and GHRH-stimulated (r2 = 0.53; P = 0.0001) GH secretion by the dispersed pituitary cells. These data suggest that a deficiency of androgen receptors results in a diminution of the in vitro GH secretory capability of anterior pituitary cells to a level below that by cells from normal males, but not to the level in normal females. The intermediate position of cells from the Tfm rat may represent a partial masculinization or defeminization within this generally female phenotype.
Authors:
J M Batson; R J Krieg; P M Martha; W S Evans
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Publication Detail:
Type:  Comparative Study; Journal Article; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Endocrinology     Volume:  124     ISSN:  0013-7227     ISO Abbreviation:  Endocrinology     Publication Date:  1989 Jan 
Date Detail:
Created Date:  1989-02-07     Completed Date:  1989-02-07     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  0375040     Medline TA:  Endocrinology     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  444-8     Citation Subset:  AIM; IM    
Affiliation:
Department of Anatomy, Medical College of Virginia, Richmond 23298.
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MeSH Terms
Descriptor/Qualifier:
Androgen-Insensitivity Syndrome / metabolism*
Animals
Cells, Cultured
Female
Growth Hormone / secretion*
Growth Hormone-Releasing Hormone / pharmacology*
Male
Perfusion
Pituitary Gland, Anterior / drug effects,  secretion*
Rats
Sex Characteristics
Grant Support
ID/Acronym/Agency:
DK-07320/DK/NIDDK NIH HHS; HD-00711/HD/NICHD NIH HHS; HD-19170/HD/NICHD NIH HHS
Chemical
Reg. No./Substance:
9002-72-6/Growth Hormone; 9034-39-3/Growth Hormone-Releasing Hormone

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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