Document Detail

The pregnancy-induced increase in baseline circulating growth hormone in rats is not induced by ghrelin.
MedLine Citation:
PMID:  18208550     Owner:  NLM     Status:  MEDLINE    
The elevation in baseline circulating growth hormone (GH) that occurs in pregnant rats is thought to arise from increased pituitary GH secretion, but the underlying mechanism remains unclear. Distribution, Fourier and algorithmic analyses confirmed that the pregnancy-induced increase in circulating GH in 3-week pregnant rats was due to a 13-fold increase in baseline circulating GH (P < 0.01), without any significant alteration in the parameters of episodic secretion. Electron microscopy revealed that pregnancy resulted in a reduction in the proportion of mammosomatotrophs (P < 0.01) and an increase in type II lactotrophs (P < 0.05), without any significant change in the somatotroph population. However, the density of the secretory granules in somatotrophs from 3-week pregnant rats was reduced (P < 0.05), and their distribution markedly polarised; the granules being grouped nearest the vasculature. Pituitary GH content was not increased, but steady-state GH mRNA levels declined progressively during pregnancy (P < 0.05). In situ hybridisation revealed that pregnancy was accompanied by a suppression of GH-releasing hormone mRNA expression in the arcuate nuclei (P < 0.05) and enhanced somatostatin mRNA expression in the periventricular nuclei (P < 0.05), an expression pattern normally associated with increased GH feedback. Although gastric ghrelin mRNA expression was elevated by 50% in 3-week pregnant rats (P < 0.01), circulating ghrelin, GH-secretagogue receptor mRNA expression and the GH response to a bolus i.v. injection of exogenous ghrelin were all largely unaffected during pregnancy. Although trace amounts of 'pituitary' GH could be detected in the placenta with radioimmunoassay, significant GH-immunoreactivity could not be observed by immunohistochemistry, indicating that rat placenta itself does not produce 'pituitary' GH. Although not excluding the possibility that the pregnancy-associated elevation in baseline circulating GH could arise from alternative extra-pituitary sources (e.g. the ovary), our data indicate that this phenomenon is most likely to result from a direct alteration of somatotroph function.
M M El-Kasti; H C Christian; I Huerta-Ocampo; M Stolbrink; S Gill; P A Houston; J S Davies; J Chilcott; N Hill; D R Matthews; D A Carter; T Wells
Publication Detail:
Type:  Comparative Study; Journal Article; Research Support, Non-U.S. Gov't     Date:  2008-01-16
Journal Detail:
Title:  Journal of neuroendocrinology     Volume:  20     ISSN:  1365-2826     ISO Abbreviation:  J. Neuroendocrinol.     Publication Date:  2008 Mar 
Date Detail:
Created Date:  2008-02-27     Completed Date:  2008-05-22     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  8913461     Medline TA:  J Neuroendocrinol     Country:  England    
Other Details:
Languages:  eng     Pagination:  309-22     Citation Subset:  IM    
School of Biosciences, Cardiff University, Museum Avenue, Cardiff, UK.
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MeSH Terms
Adiposity / physiology
Antibodies, Monoclonal / metabolism
Body Weight / physiology
Ghrelin / genetics,  metabolism,  pharmacology,  physiology*
Growth Hormone / blood*,  genetics,  metabolism,  secretion
Growth and Development / physiology
Hypothalamic Hormones / metabolism
Placenta / secretion
Pregnancy, Animal*
Rats, Sprague-Dawley
Receptors, Ghrelin / genetics,  metabolism
Somatotrophs / physiology
Time Factors
Grant Support
051887/C/97/Z//Wellcome Trust
Reg. No./Substance:
0/Antibodies, Monoclonal; 0/Ghrelin; 0/Hypothalamic Hormones; 0/Receptors, Ghrelin; 9002-72-6/Growth Hormone

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