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Horm Metab Res 2006; 38(9): 556-562
DOI: 10.1055/s-2006-950501
Original Basic

© Georg Thieme Verlag KG Stuttgart · New York

Effect of Growth Hormone in an Experimental Model of Protein Hypercatabolism Induced by Glucocorticoids

A. Cantón 1 , 2 , 3 , P. J. Trainer 1 , 4 , E. Martinez-Cáceres 5 , R. Simó 3
  • 1Department of Endocrinology, St Bartholomew's Hospital, London, UK
  • 2Department of Endocrinology, Hospital Universitari “Germans Trias i Pujol”, Badalona, Barcelona, Spain
  • 3Endocrine Division, Hospital Universitari Vall d’Hebron, Barcelona, Spain
  • 4Department of Endocrinology, Christie Hospital, Manchester, UK
  • 5Department of Immunology, LIRAD-BST, Hospital Universitari “Germans Trias I Pujol”, Badalona, Barcelona, Spain
Further Information

Publication History

Received 12 January 2006

Accepted after revision 29 May 2006

Publication Date:
18 September 2006 (online)

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Abstract

Objective: The aims of the study were to evaluate whether growth hormone could be beneficial in a model of hypercatabolism induced by glucocorticoids and to examine its effects on ACTH, corticosterone and IGF-1 levels. The effects of growth hormone on the expression of both glucocorticoid receptor and tyrosine aminotransferase were also evaluated. Methods: Fifty Wistar rats were divided into five groups and treated as follows: (A) daily subcutaneous injection of growth hormone (4.8 IU/kg/day) and oral placebo, (B) daily injection of placebo and oral dexamethasone (3 mg/kg/day), (C) daily injection of growth hormone and oral dexamethasone, (D) daily injection of placebo and oral placebo, and (E) no treatment. The animals were decapitated seven days after initiating treatment. Results: Growth hormone did not modify the weight loss induced by dexamethasone. Glucocorticoid receptor expression was significantly lower in group A than in group E. An increase in tyrosine aminotransferase was observed in group C. Conclusion: Growth hormone did not exert any beneficial effect in this model of hypercatabolism. Growth hormone decreased glucocorticoid receptor expression. This fact could explain its beneficial effect when protein hypercatabolism is not the predominant phenomenon. Growth hormone induced the hyperexpression of tyrosine aminotransferase, thus suggesting an amplifying effect on the glucocorticoid action.

Key words

Hypermetabolism - catabolism - dexamethasone - tyrosine transaminase - ACTH - corticosterone - IGF-1 levels

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Correspondence

Ana Cantón

Department of Endocrinology·Hospital Universitari “Germans Trias i Pujol”

Ctra. de Canyet, s/n·08916 Badalona·Barcelona·Spain

Phone: +34/93/497 88 60

Fax: +34/93/497 87 32

Email: acanton.germanstrias@gencat.net

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