GHRP-6
Growth Hormone Releasing Peptide-6, Growth hormone-releasing hexapeptide, His-D-Trp-Ala-Trp-D-Phe-Lys-NH2
Glucocorticoid regulation of growth hormone (GH) secretagogue-induced growth responses and GH secretagogue receptor expression in the rat.
Thomas. G B GB; Bennett. P A PA; Carmignac. D F DF; Robinson. I C IC
Key Findings
- Continuous GHRP‑6 infusion did not significantly increase weight gain in normal rats.
- Adrenalectomy (removing adrenal glands) lowered GHS‑receptor expression and blocked weight gain, but adding dexamethasone restored both receptor levels and weight gain.
- Adrenal steroids appear necessary for GHRP‑6‑induced growth responses, implying that chronic activation of the HPA axis could blunt benefits.
Practical Outcomes
- For biohackers, this means that long‑term, high‑dose GHRP‑6 may not boost muscle or weight unless cortisol levels are adequate, and continuous dosing could even be counter‑productive. Consider using intermittent dosing schedules and monitoring adrenal function (e.g., cortisol) if you plan to use GHRP‑6 for growth or body‑composition goals.
Summary
In rats, giving GHRP‑6 continuously didn’t make them gain much weight unless their adrenal glands (which make cortisol) were working or were replaced with dexamethasone. Without adrenal steroids, the receptors for GHRP‑6 dropped, and the peptide couldn’t boost growth. This suggests that the hormone environment matters a lot for GHRP‑6’s effects.
Abstract
Synthetic GH-releasing peptides such as GHRP-6 are potent GH secretagogues (GHSs) in several species, but attempts to stimulate growth by continuous GHS exposure have had limited success. GHSs also release ACTH and adrenal steroids. Since glucocorticoid excess is associated with poor linear growth, stimulation of the hypothalamo-pituitary-adrenal (HPA) axis by continuous GHS administration may compromise their growth-promoting effects. We have now examined the effects of continuous GHRP-6 infusion (100 mg/day, s.c. for 14 days) in normal 150-day-old female rats, and in adrenalectomized (Adx) rats with or without dexamethasone (Dex) replacement. Infusion of GHRP-6 did not significantly affect body weight gain compared with excipient-treated controls in either intact rats (controls, 9.0 +/- 1.6 vs GHRP-6, 11.8 +/- 0.9 g) or Adx rats (4.4 +/- 1.5 vs 7.9 +/- 2.7 g). However, GHRP-6 significantly increased weight gain in Adx rats treated with Dex (controls, 3.5 +/- 1.4 vs GHRP-6, 15.4 +/- 1.6 g;P<0.01). Adrenalectomy decreased plasma triglycerides (P<0.01), and Dex treatment increased plasma cholesterol (P<0.001), GHRP-6 treatment did not affect these plasma lipids. Dex treatment also reduced plasma GH-binding protein levels and hepatic GH binding (P<0.05). Pituitary GH content was decreased in Adx rats (P<0.05) but not in Dex-treated Adx rats. Adrenalectomy markedly decreased GHS-receptor mRNA expression in the arcuate (P<0. 001) and ventromedial nuclei (P<0.01), whilst Dex treatment normalized GHS-receptor expression. These results suggest that adrenal steroids are necessary for normal GHS-receptor expression and GHRP-6-induced weight gain, but long-term stimulation of the HPA axis by continuous GHS exposure may be detrimental to the growth response.
Study Information
pubmed
2000
10.1054/ghir.1999.0138