GHRP-6
Growth Hormone Releasing Peptide-6, Growth hormone-releasing hexapeptide, His-D-Trp-Ala-Trp-D-Phe-Lys-NH2
Ghrelin enhancer, rikkunshito, improves postprandial gastric motor dysfunction in an experimental stress model.
Harada. Y Y; Ro. S S; Ochiai. M M; Hayashi. K K; Hosomi. E E; Fujitsuka. N N; Hattori. T T; Yakabi. K K
Key Findings
- Stress (via urocortin1) lowers plasma acylated ghrelin and delays gastric emptying in the animal model.
- Injecting acylated ghrelin or giving rikkunshito restores normal gastric emptying and improves antral motility.
- The positive effect of rikkunshito is blocked by a ghrelin‑receptor antagonist, confirming it works through ghrelin signaling.
Practical Outcomes
- For biohackers, this suggests that ghrelin‑boosting strategies—like using GHRP‑6 or the herbal formula rikkunshito—might help counter stress‑related digestive slowdown. However, the study is in animals, so human dosing and safety need more research before routine use.
Summary
In stressed animals, the hormone ghrelin drops, causing slower stomach emptying and messed‑up gut movements. Giving extra ghrelin or a herbal mix called rikkunshito (which boosts the body's own ghrelin) fixes the stomach’s speed and normalises gut muscle activity. The benefit disappears if the ghrelin receptor is blocked, showing the effect depends on ghrelin signaling.
Abstract
Functional dyspepsia (FD) is one of the most common disorders of gastrointestinal (GI) diseases. However, no curable treatment is available for FD because the detailed mechanism of GI dysfunction in stressed conditions remains unclear. We aimed to clarify the association between endogenous acylated ghrelin signaling and gastric motor dysfunction and explore the possibility of a drug with ghrelin signal-enhancing action for FD treatment. Solid gastric emptying (GE) and plasma acylated ghrelin levels were evaluated in an urocortin1 (UCN1) -induced stress model. To clarify the role of acylated ghrelin on GI dysfunction in the model, exogenous acylated ghrelin, an endogenous ghrelin enhancer, rikkunshito, or an α2 -adrenergic receptor (AR) antagonist was administered. Postprandial motor function was investigated using a strain gauge force transducer in a free-moving condition. Exogenous acylated ghrelin supplementation restored UCN1-induced delayed GE. Alpha2 -AR antagonist and rikkunshito inhibited the reduction in plasma acylated ghrelin and GE in the stress model. The action of rikkunshito on delayed GE was blocked by co-administration of the ghrelin receptor antagonist. UCN1 decreased the amplitude of contraction in the antrum while increasing it in the duodenum. The motility index of the antrum but not the duodenum was significantly reduced by UCN1 treatment, which was improved by acylated ghrelin or rikkunshito. The UCN1-induced gastric motility dysfunction was mediated by abnormal acylated ghrelin dynamics. Supplementation of exogenous acylated ghrelin or enhancement of endogenous acylated ghrelin secretion by rikkunshito may be effective in treating functional GI disorders.
Study Information
pubmed
2015
2015-06-18T00:00:00.000Z
10.1111/nmo.12588
14
52