Study summary · research use only
Acute dexamethasone administration enhances GH responsiveness to GH releasing peptide-6 (GHRP-6) in man
Plain-language summary
Paraphrased from the published abstract below — not a verdict on whether anything works.
This human study evaluated whether acute oral dexamethasone alters GH responsiveness to the synthetic hexapeptide GHRP-6. Sixteen normal subjects (mean age 29 years, normal BMI) were studied; eight received dexamethasone (4 mg) and eight received placebo, 3.5 hours before intravenous GHRP-6 (1 microg/kg), GH-releasing hormone (GHRH; 100 microg), both peptides together, or saline. The authors report that after placebo, peak GH and area-under-the-curve values after GHRP-6 did not differ from those after GHRH, while the two peptides combined markedly increased GH levels. After dexamethasone, GH responsiveness to GHRP-6 was significantly greater than after placebo, whereas responses to GHRH or to the combined peptides did not differ between groups. The authors suggest dexamethasone and GHRP-6 may act at different sites, and note further studies are needed.
Abstract
Acute administration of glucocorticoids stimulates GH secretion probably by a decrease in hypothalamic somatostatin release. GHRP-6 is a synthetic hexapeptide that increases GH secretion by a mechanism of action not yet fully known, but apparently not by inhibition of hypothalamic somatostatin release. The aim of this study was to evaluate the effect of acute dexamethasone administration on GH responsiveness to GHRP-6 in man. One group of subjects received iv GHRP-6 (1 microg/kg), GH-releasing hormone (GHRH; 100 microg), GHRH plus GHRP-6 or saline 3.5 h after oral acute dexamethasone administration (4 mg; at 0600 h). A second study group was treated with GHRP-6, GHRH or GHRP-6 plus GHRH after placebo ingestion, following the same protocol. Sixteen normal subjects (mean age: 29 +/- 3.3 years), with normal BMI (22.4 +/- 2.0 kg/m2), were studied. Eight subjects received dexamethasone and the other eight were treated with placebo. Serum GH was measured by a two site monoclonal antibody immunofluorometric assay. In the placebo-treated subjects, mean peak GH (mU/l; mean +/- SE) and AUC (mU.min/l) values after GHRP-6 administration (peak: 43.8 +/- 9.0; AUC: 2262.0 +/- 459. 2) did not differ from those observed after GHRH injection (peak: 49. 8 +/- 12.0; AUC: 2903.4 +/- 872.6). The association of the two peptides markedly increased GH levels (peak: 172.4 +/- 34.2; AUC: 10393.0 +/- 1894.8) compared with the isolated administration of GHRP-6 or GHRH. In the subjects who received dexamethasone 3.5 h before saline injection, GH baseline values were significantly higher than those observed after 90 min of sampling (12.4 +/- 9.4 vs. 4.6 +/- 2.0). Mean GH peak and AUC values after GHRP-6 (peak: 78.8 +/- 11.0; AUC: 4114.6 +/- 588.2) and after GHRH administration (peak: 46.8 +/- 16.0; AUC: 3006.8 +/- 1010.0) did not differ significantly in the dexamethasone-treated subjects. In this study group, the administration of the two peptides together caused a significant increase in both peak (119.2 +/- 16.0) and AUC values (7377.0 +/- 937.2) compared with the response obtained after each peptide alone. When the two groups were compared, a significant increase in GH responsiveness to GHRP-6 was observed after dexamethasone administration compared with placebo. No differences in GH response to GHRH, or to the administration of the two peptides together, were seen between the two groups. Oral dexamethasone, at a dose of 4 mg, enhances GH releasing peptide-6-induced GH release when administered 3.5 h earlier. These results suggest that dexamethasone and GHRP-6 could act at different sites of GH releasing mechanisms. Further studies are necessary to elucidate these findings.
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