GHRP-6
Growth Hormone Releasing Peptide-6, Growth hormone-releasing hexapeptide, His-D-Trp-Ala-Trp-D-Phe-Lys-NH2
Regulation of His-dTrp-Ala-Trp-dPhe-Lys-NH2 (GHRP-6)-induced GH secretion in the rat.
Mallo. F F; Alvarez. C V CV; Benitez. L L; Burguera. B B; Coya. R R; Casanueva. F F FF; Dieguez. C C
Key Findings
- GHRP-6 directly stimulates GH release from the pituitary, independent of hypothalamic input.
- Sex hormones (estrogen and testosterone) enhance the GH response to GHRP-6.
- Elevated cortisol (via dexamethasone), high free fatty acids, or bombesin sharply blunt the GH response.
- Chronic pre‑treatment with GHRP‑6 or GHRH does not alter the acute GH‑releasing effect.
Practical Outcomes
- For biohackers, GHRP‑6 can be used as a GH‑releasing agent, but its effectiveness may be higher when cortisol levels are low and when sex hormone status is optimal. Avoid dosing right after high‑fat meals or during periods of stress that raise cortisol, as these conditions can dampen the GH surge. The study doesn’t suggest a need for long‑term priming doses before using GHRP‑6.
Summary
In rats, the peptide GHRP-6 reliably triggers a spike in growth hormone (GH) even when the brain's usual control centers are removed, showing it works directly on the pituitary gland. The hormone boost is stronger in animals given estrogen or testosterone, but weaker when cortisol (from dexamethasone), high blood fats, or bombesin are present. Repeated GHRP-6 dosing for two weeks doesn’t change the acute GH response.
Abstract
His-dTrp-Ala-Trp-dPhe,Lys-NH2(GHRP-6) is a synthetic compound that releases GH in a dose-response and specific manner in several species and that may well be related to an endogenous compound of similar structure. The aim of this study was to investigate the in vivo GH responses to GHRP-6 in pentobarbital anesthetized rats. Specifically and in order to avoid the influence of endogenous GHRH and somatostatin secretion we studied the GH responses to GHRP-6 in animals with surgical ablation of the hypothalamus, confirmed by histological assessment, as well as in hypophysectomyzed-transplanted rats bearing two hypophyses under the renal capsule. Since it has been previously reported that rats pretreated with GHRH (10 micrograms/kg i.p. every 12 h for 15 days) rather than saline-treated rats have greater GH responses to acutely administered GHRH, we compared the self-potentiating effect of chronic GH pretreatment with GHRP-6 (10 micrograms/kg i.p. every 12 h). Furthermore we also studied the influence of estrogens, glucocorticoids, free fatty acids (FFA) and bombesin on somatotroph responsiveness to GHRP-6 in intact rats. We found a greater GH response to GHRP-6 in rats that underwent a surgical ablation of the hypothalamus 36 h prior to the test than in sham-operated rats. A direct stimulatory effect of GHRP-6 on in vivo GH secretion was demonstrated by a clear GH response to GHRP-6 in hypophysectomyzed-transplanted rats. In addition, we found a similar response whether the animals were pretreated with GHRH or GHRP-6 over the previous 2 weeks. Finally, we found that both estrogen- and testosterone-treated rats have greater GH responses to GHRP-6 than untreated rats. On the other hand, chronic dexamethasone administration, acute elevation of circulating FFA levels and bombesin administration markedly inhibited GH responses to GHRP-6. In contrast to the effects exerted on GH responses to GHRP-6 estrogen administration led to a decrease in GH responses to GHRH while dexamethasone did not affect the GH responses to GHRH, highlighting a differential regulation of these hormones on somatotroph responsiveness to these peptides.
Study Information
pubmed
1993
10.1159/000126366
62