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GHRP-6

Growth Hormone Releasing Peptide-6, Growth hormone-releasing hexapeptide, His-D-Trp-Ala-Trp-D-Phe-Lys-NH2

Quick Stats
Studies 702
Trials 0
Score 2
2013 pubmed 20 citations

Interruption of ghrelin signaling in the PVN increases high-fat diet intake and body weight in stressed and non-stressed C57BL6J male mice.

Patterson. Zachary R ZR; Parno. Tamara T; Isaacs. Albert M AM; Abizaid. Alfonso A

Key Findings

  • Antagonizing the ghrelin receptor in the PVN increased high‑fat diet intake in both stressed and non‑stressed mice.
  • Ghrelin signaling in the PVN appears to favor carbohydrate‑rich foods and suppress fat consumption.
  • The effect was observed with a specific ghrelin receptor antagonist ([D‑Lys‑3]‑GHRP‑6) delivered directly to the brain, not with systemic administration.

Practical Outcomes

  • For biohackers using GHRP‑6 to boost growth hormone, the study hints that activating ghrelin receptors might shift food cravings toward carbs and away from fat, but the evidence is limited to mice and a brain‑targeted delivery method. It does not provide a clear dosage or protocol for humans, so any dietary effects should be considered speculative and monitored individually.

Summary

A mouse study found that blocking ghrelin receptors in a brain area called the PVN made the animals eat more high‑fat food, especially when they were stressed. This suggests that normal ghrelin signaling may steer eating toward carbs and away from fat. The research used a ghrelin‑blocking peptide (a version of GHRP‑6) and did not test the effects of the usual GHRP‑6 agonist that many biohackers use.

Abstract

Chronic social stress has been associated with increased caloric intake and adiposity. These effects have been linked to stress induced changes in the secretion of ghrelin, a hormone that targets a number of brain regions to increase food intake and energy expenditure and promote increased body fat content. One of the brain sites targeted by ghrelin is the hypothalamic paraventricular nucleus (PVN), a region critical for both the regulation of the stress response and the regulation of energy balance. Given these data, we examined the contribution of ghrelin receptors in the PVN to the metabolic and behavioral changes that are seen during chronic social stress in mice. To do this, mice were implanted with cannulae attached to osmotic minipumps and delivering either vehicle or the ghrelin receptor (growth hormone secretagogue receptor) antagonist [D-Lys-3]-GHRP-6 (20 nmol/day/mouse). Following a week of recovery, half of the animals in each group were exposed to chronic social defeat stress for a period of 3 weeks whereas the other half were left undisturbed. During this time, all animals were given ad libitum access to standard laboratory chow and presented a high-fat diet for 4 h during the day. Results showed that the ghrelin receptor antagonism did not decrease stressed induced caloric intake, but paradoxically increased the intake of the high fat diet. This would suggest that ghrelin acts on the PVN to promote the intake of carbohydrate rich diets while decreasing fat intake and blockade of ghrelin receptors in the PVN leads to more consumption of foods that are high in fat.

Study Information

Provider

pubmed

Year

2013

Date

2013-09-17T00:00:00.000Z

DOI

10.3389/fnins.2013.00167

Citations

20

References

40