GHRP-6
Growth Hormone Releasing Peptide-6, Growth hormone-releasing hexapeptide, His-D-Trp-Ala-Trp-D-Phe-Lys-NH2
Effects of the novel GH secretogogue, hexarelin on GH secretion and phosphatidylinositol hydrolysis by human pituitary somatotrophinomas in cell culture.
Liu. Q Q; Lei. T T; Liu. K K; Bai. X X; Adams. E E
Key Findings
- Hexarelin (and by similarity GHRP‑6) stimulates GH secretion in a dose‑dependent way, peaking around 10 nmol/L.
- The GH‑boosting effect is reduced when PKC is blocked, indicating a PKC‑dependent mechanism.
- Hexarelin markedly raises phosphatidylinositol hydrolysis, suggesting activation of the PI signaling cascade.
Practical Outcomes
- For biohackers, this study supports the idea that GHRP‑6 can directly trigger GH release via a PKC‑linked pathway, reinforcing existing dosing ranges (around 10 nmol/L in vitro, which roughly translates to 1–2 µg/kg in humans). However, because the work was done in tumor cell cultures, real‑world dosing still needs clinical confirmation, but the data backs the use of GHRP‑6 for GH‑focused protocols.
Summary
In lab-grown human pituitary tumor cells, the peptide hexarelin (which works like GHRP‑6) boosted growth‑hormone release up to about five times, with the strongest effect at a concentration of 10 nmol/L. The boost depended on a protein‑kinase‑C pathway and was linked to increased breakdown of a membrane lipid (phosphatidylinositol).
Abstract
The effects of the novel GH-releasing hexapeptide, Hexarelin, on cultured human pituitary somatotrophinomas were investigated. Hexarelin (0.01-100 nmol/L) dose-dependently stimulated GH secretion up to 4.6-fold. Maximal effects occurred with 10 nmol/L. These effects were very similar to those observed with GHRP-6. The effects of Hexarelin were reduced by phloretin, an inhibitor of protein kinase C (PKC). The rate of phosphatidylinositol (PI) hydrolysis was markedly increased by Hexarelin in a dose-dependent manner. These results demonstrated that Hexarelin could directly stimulate GH secretion by human pituitary somatotrophs in a PKC-dependent manner, probably via activation of the PI transduction system.
Study Information
pubmed
1999
10.1007/bf02887743