Growth hormone axis in cushing's syndrome

• Published in: Hormone research Vol. 45; no. 1-2; p. 99
• Main Authors: Wajchenberg, B L, Liberman, B, Giannella Neto, D, Morozimato, M Y, Semer, M, Bracco, L O, Salgado, L R, Knoepfelmacher, M, Borges, M H, Pinto, A C, Kater, C E, Lengyel, A M
• Format: Journal Article
• Language: English
• Published: Switzerland 01.01.1996
• Subjects: Carrier Proteins - physiology; Cushing Syndrome - physiopathology; Female; Growth Hormone - blood; Growth Hormone - physiology; Growth Hormone - secretion; Growth Hormone-Releasing Hormone; Humans; Insulin-Like Growth Factor Binding Proteins - physiology; Insulin-Like Growth Factor I - physiology; Male; Models, Biological; Reference Values
• ISSN: 0301-0163; 1423-0046
• DOI: 10.1159/000184767

All 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.