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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 3
2011 pubmed 22 citations

Ghrelin agonists impact on Fos protein expression in brain areas related to food intake regulation in male C57BL/6 mice.

Pirnik. Z Z; Bundziková. J J; Holubová. M M; Pýchová. M M; Fehrentz. J A JA; Martinez. J J; Zelezná. B B; Maletínská. L L; Kiss. A A

Key Findings

  • All three ghrelin agonists (including GHRP‑6) raised Fos protein levels in key hunger‑regulating brain regions (PVN, ARC, NTS, AP).
  • The pattern of neuronal activation was similar across different agonists despite their distinct chemical structures.
  • A single sub‑cutaneous dose (5 mg/kg) that increased food intake also produced widespread activation of appetite‑related neurons.

Practical Outcomes

  • For the biohacker community, the data backs the use of GHRP‑6 as an appetite‑stimulating tool, but remember the study was done in mice at a high dose. Start with low, human‑appropriate doses, watch for side effects, and understand that human efficacy still needs more research.

Summary

In mice, injecting the ghrelin‑like peptide GHRP‑6 (and similar compounds) sparked activity in brain areas that control hunger, which led to a noticeable increase in food intake. This shows that GHRP‑6 can act as a strong appetite stimulant, suggesting it might help people who need to boost their eating, such as during weight‑loss or muscle‑building phases.

Abstract

Many peripheral substances, including ghrelin, induce neuronal activation in the brain. In the present study, we compared the effect of subcutaneously administered ghrelin and its three stable agonists: Dpr(3)ghr ([Dpr(N-octanoyl)(3)] ghrelin) (Dpr - diaminopropionic acid), YA GHRP-6 (H-Tyr-Ala-His-DTrp-Ala-Trp-DPhe-Lys-NH(2)), and JMV1843 (H-Aib-DTrp-D-gTrp-CHO) on the Fos expression in food intake-responsive brain areas such as the hypothalamic paraventricular (PVN) and arcuate (ARC) nuclei, the nucleus of the solitary tract (NTS), and area postrema (AP) in male C57BL/6 mice. Immunohistochemical analysis showed that acute subcutaneous dose of each substance (5mg/kg b.w.), which induced a significant food intake increase, elevated Fos protein expression in all brain areas studied. Likewise ghrelin, each agonist tested induced distinct Fos expression overall the PVN. In the ARC, ghrelin and its agonists specifically activated similarly distributed neurons. Fos occurrence extended from the anterior (aARC) to middle (mARC) ARC region. In the latter part of the ARC, the Fos profiles were localized bilaterally, especially in the ventromedial portions of the nucleus. In the NTS, all substances tested also significantly increased the number of Fos profiles in neurons, which also revealed specific location, i.e., in the NTS dorsomedial subnucleus (dmNTS) and the area subpostrema (AsP). In addition, cells located nearby the NTS, in the AP, also revealed a significant increase in number of Fos-activated cells. These results demonstrate for the first time that ghrelin agonists, regardless of their different chemical nature, have a significant and similar activating impact on specific groups of neurons that can be a part of the circuits involved in the food intake regulation. Therefore there is a real potency for ghrelin agonists to treat cachexia and food intake disorders. Thus, likewise JMV1843, the other ghrelin agonists represent substances that might be involved in trials for clinical purposes.

Study Information

Provider

pubmed

Year

2011

Date

2011-08-06T00:00:00.000Z

DOI

10.1016/j.neuint.2011.08.001

Citations

22

References

63