GHRP-6
Growth Hormone Releasing Peptide-6, Growth hormone-releasing hexapeptide, His-D-Trp-Ala-Trp-D-Phe-Lys-NH2
Sulfated gastrin stimulates ghrelin and growth hormone release but inhibits insulin secretion in cattle.
Zhao. Hongqiong H; Yannaing. Swe S; Thanthan. Sint S; Kuwayama. Hideto H
Key Findings
- Sulfated gastrin dose‑dependently increased both acyl and total ghrelin in the bloodstream.
- Growth hormone levels rose after gastrin injection, but the highest dose was less effective than a mid‑range dose.
- Insulin concentrations fell quickly after gastrin and stayed low, while glucagon and glucose were unchanged.
- Blocking the GHS‑R1a receptor with [D‑Lys(3)]‑GHRP‑6 did not prevent gastrin‑induced growth hormone release.
Practical Outcomes
- For biohackers, the study hints that gastrin or related compounds could boost GH and lower insulin, but the animal model and huge doses limit direct use in humans. It suggests that GHRP‑6 may not be necessary for GH elevation via gastrin pathways, and any experimentation should proceed with caution and further human‑focused research.
Summary
In a study on cows, giving a form of gastrin (a stomach hormone) caused both ghrelin and growth hormone levels to go up, while insulin dropped and stayed low. Blocking the usual ghrelin receptor with a GHRP‑6 variant didn’t stop the growth hormone rise, meaning gastrin may trigger growth hormone through a different route. The findings are interesting but come from cattle and use very high doses, so they don’t directly translate into a human protocol.
Abstract
This study was designed to determine the effects of gastrin on the circulating levels of ghrelin, growth hormone (GH), insulin, glucagon and glucose in ruminants. Two experiments were done in eight Holstein steers. Animals were randomly assigned to receive intravenous bolus injections: (1) 0.1% bovine serum albumin in saline as vehicle, 0.8, 4.0 and 20.0 μg/kg body weight (BW) of bovine sulfated gastrin-34; (2) vehicle, 0.53 μg/kg BW of bovine sulfated gastrin-17 alone or combined with 20.0 μg/kg BW of [D-Lys(3)]-GHRP-6, the selective antagonist of GHS-R1a. Blood samples were collected from -10 to 150 min relative to injection time. Concentrations of acyl and total ghrelin in response to gastrin-34 injection were significantly increased in a dose-dependent manner. Concentrations of GH were also markedly elevated by gastrin-34 injection; however, the effect of 20.0 μg/kg was weaker than that of 4.0 μg/kg. The three doses of gastrin-34 equally decreased insulin levels within 15 min and maintained the level until the time of last sampling. Gastrin-34 had no effect (P > 0.05) on the levels of glucagon and glucose. Levels of acyl ghrelin increased after administration of gastrin-17 alone or combined with [D-Lys(3)]-GHRP-6; however, [D-Lys(3)]-GHRP-6 did not block the elevation of GH by gastrin-17. The present results indicate that sulfated gastrin stimulates both ghrelin and GH release, but the GHS-R1a may not contribute to the release of GH by gastrin. Moreover, sulfated gastrin seems to indirectly maintain the homeostasis of blood glucose through the down-regulation of insulin in ruminants.
Study Information
pubmed
2011
2011-10-06T00:00:00.000Z
10.1016/j.peptides.2011.09.023
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