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dc.contributor.authorCantón, A
dc.contributor.authorTrainer, Peter J
dc.contributor.authorMartinez-Cáceres, E
dc.contributor.authorSimó, R
dc.date.accessioned2009-07-06T14:52:24Z
dc.date.available2009-07-06T14:52:24Z
dc.date.issued2006-09
dc.identifier.citationEffect of growth hormone in an experimental model of protein hypercatabolism induced by glucocorticoids. 2006, 38 (9):556-62 Horm. Metab. Res.en
dc.identifier.issn1439-4286
dc.identifier.pmid16981136
dc.identifier.doi10.1055/s-2006-950501
dc.identifier.urihttp://hdl.handle.net/10541/72616
dc.description.abstractOBJECTIVE: 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.
dc.language.isoenen
dc.subject.meshAdrenocorticotropic Hormone
dc.subject.meshAnimals
dc.subject.meshBody Weight
dc.subject.meshCorticosterone
dc.subject.meshDexamethasone
dc.subject.meshDisease Models, Animal
dc.subject.meshGene Expression Regulation
dc.subject.meshGlucocorticoids
dc.subject.meshHuman Growth Hormone
dc.subject.meshInsulin-Like Growth Factor I
dc.subject.meshMale
dc.subject.meshMetabolic Diseases
dc.subject.meshProteins
dc.subject.meshRats
dc.subject.meshRats, Wistar
dc.subject.meshReceptors, Glucocorticoid
dc.subject.meshTyrosine Transaminase
dc.titleEffect of growth hormone in an experimental model of protein hypercatabolism induced by glucocorticoids.en
dc.typeArticleen
dc.contributor.departmentDepartment of Endocrinology, St Bartholomew's Hospital, London, UK. acanton.germanstrias@gencat.neten
dc.identifier.journalHormone and Metabolic Researchen
html.description.abstractOBJECTIVE: 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.


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