B.L. Wajchenberg a , B. Liberman a , Giannella Neto a , M.Y. Morozimato a , M. Semer a , L.O. Bracco a , L.R. Salgado a , M. Knoepfelmacher a , M.H.S. Borges b , A.C.A.R. Pinto b , C.E. Kater b , A.M.J. Lengyel b
09 December 2008
All levels of the growth hormone (GH), GH binding protein (GHBP), insulinlike 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.