GROWTH-HORMONE AXIS IN CUSHINGS-SYNDROME

All levels of the growth hormone (GH), GH binding protein (GHBP), insu lin-like growth factor (IGF) and IGF binding protein (IGFBP) axis are influenced by chronic hypercortisolism. Thus, there is a blunted respo nse to GHRH alone or together with other stimuli associated with a mar ked suppression of endogenous GH secretion but accompanied by normal G HBP, 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 t o normal. These findings may suggest enhanced GH sensitivity with norm al or increased IGF-1 bioavailability to the correspondent tissue rece ptors. In conclusion, the glucocorticoid (GC)-induced target tissue re sistance can neither be attributed to the suppression of the GH axis n or 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 p ostbinding IGF-1 bioactivity (gene expression) and/or by the downmodul ation of activator protein-1 (Fos/Jun) activity by the GC-GC receptor complex.