HOME HELP CONTACT US SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Flint, D. J Articles by Kelly, P. Search for Related Content PubMed PubMed Citation Articles by Flint, D. J Articles by Kelly, P.

¹ Department of Bioscience, University of Strathclyde, Glasgow G1 1XW, UK
² Inserm U809, Faculté de Médecine René Descartes- site Necker, Université Paris Descartes, F-75015 Paris, France
³ College of Osteopathic Medicine, Edison Biotechnology Institute, Ohio University, Athens, Ohio 45701, USA

(Requests for offprints should be addressed to D J Flint; Email: david.flint{at}strath.ac.uk)

Direct metabolic effects of GH on adipose tissue are well established, but effects of prolactin (PRL) have been more controversial. Recent studies have demonstrated PRL receptors on adipocytes and effects of PRL on adipose tissue in vitro. The role of GH in adipocyte proliferation and differentiation is also controversial, since GH stimulates adipocyte differentiation in cell lines, whereas it stimulates proliferation but inhibits differentiation of adipocytes in primary cell culture. Using female gene disrupted (ko) mice, we showed that absence of PRL receptors (PRLRko) impaired development of both internal and s.c. adipose tissue, due to reduced numbers of adipocytes, an effect differing from that of reduced food intake, where cell volume is decreased. In contrast, GHRko mice exhibited major decreases in the number of internal adipocytes, whereas s.c. adipocyte numbers were increased, even though body weight was decreased by 40–50%. The changes in adipose tissue in PRLRko mice appeared to be entirely due to extrinsic factors since preadipocytes proliferated and differentiated in similar fashion to wild-type animals in vitro and their response to insulin and isoproterenol was similar to wild-type animals. This contrasted with GHRko mice, where s.c. adipocytes proliferated, differentiated, and responded to hormones in identical fashion to controls, whereas parametrial adipocytes exhibited markedly depressed proliferation and differentiation potential and failed to respond to insulin or noradrenaline. Our results provide in vivo evidence that both GH and PRL stimulate differentiation of adipocytes but that the effects of GH are site specific and induce intrinsic changes in the precursor population, which are retained in vitro.

This article has been cited by other articles:

				D. E. Berryman, E. O. List, A. J. Palmer, M.-Y. Chung, J. Wright-Piekarski, E. Lubbers, P. O'Connor, S. Okada, and J. J. Kopchick Two-Year Body Composition Analyses of Long-Lived GHR Null Mice J Gerontol A Biol Sci Med Sci, January 1, 2010; 65A(1): 31 - 40. [Abstract] [Full Text] [PDF]

				N. Ben-Jonathan, C. R. LaPensee, and E. W. LaPensee What Can We Learn from Rodents about Prolactin in Humans? Endocr. Rev., February 1, 2008; 29(1): 1 - 41. [Abstract] [Full Text] [PDF]

				J. S. Davies, E. F. Gevers, A. E. Stevenson, K. T. Coschigano, M. M. El-Kasti, M. J. Bull, C. Elford, B. A. J. Evans, J. J. Kopchick, and T. Wells Adiposity profile in the dwarf rat: an unusually lean model of profound growth hormone deficiency Am J Physiol Endocrinol Metab, May 1, 2007; 292(5): E1483 - E1494. [Abstract] [Full Text] [PDF]