Exogenous growth hormone inhibits growth hormone-releasing factor-induced growth hormone secretion in normal men

• Published in: The Journal of clinical investigation Vol. 77; no. 1; pp. 176 - 180
• Main Authors: Rosenthal, S M, Hulse, J A, Kaplan, S L, Grumbach, M M
• Format: Journal Article
• Language: English
• Published: Ann Arbor, MI American Society for Clinical Investigation 01.01.1986
• Subjects: Adult; Biological and medical sciences; Feedback; Growth Hormone - analogs & derivatives; Growth Hormone - antagonists & inhibitors; Growth Hormone - blood; Growth Hormone - pharmacology; Growth Hormone - secretion; Growth Hormone-Releasing Hormone - administration & dosage; Growth Hormone-Releasing Hormone - pharmacology; Hormones - pharmacology; Hormones. Endocrine system; Human Growth Hormone; Humans; Male; Medical sciences; Peptide Fragments - administration & dosage; Peptide Fragments - pharmacology; Pharmacology. Drug treatments; Recombinant Proteins - pharmacology; Somatomedins - biosynthesis; Somatomedins - blood; Human; Protein hormone; Hypothalamus; STH; Peptide hormone; STH-RH
• ISSN: 0021-9738
• DOI: 10.1172/JCI112273

Previous studies from this laboratory and by others in rats, monkeys, and humans support the concept that growth hormone (GH) can regulate its own secretion through an autofeedback mechanism. With the availability of human growth hormone-releasing factor (GRF), the possible existence of such a mechanism was reexplored by examining the effect of exogenous GH on the GH response induced by GRF-44-NH2 in six normal men (mean age, 32.4 yr). In all subjects the plasma GH response evoked by GRF-44-NH2 (1 microgram/kg i.v. bolus) was studied before and after 5 d of placebo (1 ml normal saline i.m. every 12 h), and then before and 12 h after 5 d of biosynthetic methionyl human GH (5 U i.m. every 12 h). The GH response to GRF (maximal increment over time 0 value) was significantly inhibited after GH treatment (0-1.3 vs. 2.3-11.2 ng/ml before treatment, P = 0.05), but was not significantly affected by placebo. This impaired pituitary response to GRF persisted for at least 24 h following exogenous GH treatment in two subjects who underwent further study. Serum somatomedin-C concentrations were significantly increased after 5 d of GH treatment (2.66-5.00 vs. 0.92-1.91 U/ml before treatment, P = less than 0.01). The impaired pituitary response to GRF may be mediated indirectly through somatomedin, somatostatin, by a direct effect of GH on the pituitary somatotropes, or by all of these mechanisms. These data suggest that after GH treatment, the blunted GH response to synthetic GRF is not solely a consequence of the inhibition of hypothalamic GRF secretion.