Growth hormone axis in Cushing's syndrome

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dc.contributor.authorWajchenberg, B. L.
dc.contributor.authorLiberman, B.
dc.contributor.authorNeto, D. G.
dc.contributor.authorMorozimato, M. Y.
dc.contributor.authorSemer, M.
dc.contributor.authorBracco, L. O.
dc.contributor.authorSalgado, L. R.
dc.contributor.authorKnoepfelmacher, M.
dc.contributor.authorBorges, MHS
dc.contributor.authorPinto, ACAR
dc.contributor.authorKater, C. E.
dc.contributor.authorLengyel, AMJ
dc.contributor.institutionUniversidade Federal de São Paulo (UNIFESP)
dc.date.accessioned2018-06-15T17:35:08Z
dc.date.available2018-06-15T17:35:08Z
dc.date.issued1996-01-01
dc.description.abstractAll levels of the growth hormone (GH), GH binding protein (GHBP), insulin-like growth factor (IGF) and IGF binding protein (IGFBP) axis are influenced by chronic hypercortisolism. Thus, there is a blunted response to GHRH alone or together with other stimuli associated with a marked suppression of endogenous GH secretion but accompanied by normal GHBP, normal to low IGF-1 and GHBPs 1 and 3 with the correspondent 41.5 and 38.5-kD molecular forms of the latter presenting values similar to normal. These findings may suggest enhanced GH sensitivity with normal or increased IGF-1 bioavailability to the correspondent tissue receptors. In conclusion, the glucocorticoid (GC)-induced target tissue resistance can neither be attributed to the suppression of the GH axis nor to changes in circulating GHBPs 1 and 3. However, it may be related either to the described 12- to-20-kD inhibitor(s) which antagonizes postbinding IGF-1 bioactivity (gene expression) and/or by the downmodulation of activator protein-1 (Fos/Jun) activity by the GC-GC receptor complex.en
dc.description.affiliationFED UNIV SAO PAULO,ESCOLA PAULISTA MED,DIV ENDOCRINOL,SAO PAULO,BRAZIL
dc.description.affiliationUnifespFED UNIV SAO PAULO,ESCOLA PAULISTA MED,DIV ENDOCRINOL,SAO PAULO,BRAZIL
dc.description.sourceWeb of Science
dc.format.extent99-107
dc.identifierhttps://doi.org/10.1159/000184767
dc.identifier.citationHormone Research. Basel: Karger, v. 45, n. 1-2, p. 99-107, 1996.
dc.identifier.doi10.1159/000184767
dc.identifier.issn0301-0163
dc.identifier.urihttp://repositorio.unifesp.br/handle/11600/43801
dc.identifier.wosWOS:A1996TV18500016
dc.language.isoeng
dc.publisherKarger
dc.relation.ispartofHormone Research
dc.rightsinfo:eu-repo/semantics/restrictedAccess
dc.rights.licensehttp://www.karger.com/Services/RightsPermissions
dc.subjectCushing's syndromeen
dc.subjectsecretion, growth hormoneen
dc.subjectinsulin-like growth factor-1en
dc.subjectbinding proteinsen
dc.subjectmolecular forms, binding proteinsen
dc.titleGrowth hormone axis in Cushing's syndromeen
dc.typeinfo:eu-repo/semantics/article
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