GHRP-6
Growth Hormone Releasing Peptide-6, Growth hormone-releasing hexapeptide, His-D-Trp-Ala-Trp-D-Phe-Lys-NH2
Ghrelin system in pancreatic AR42J cells: its ligand stimulation evokes calcium signalling through ghrelin receptors.
Lai. Jan Kit Ching JK; Cheng. Christopher H K CH; Ko. Wing Hung WH; Leung. Po Sing PS
Key Findings
- AR42J pancreatic cells consistently express both ghrelin and its receptor.
- Ghrelin and the peptide GHRP‑6 trigger a biphasic increase in intracellular calcium in these cells.
- The calcium response is stopped by receptor antagonists and calcium channel blockers, showing the pathway depends on ghrelin receptors and calcium influx.
Practical Outcomes
- At present there’s no direct protocol or dosage guidance for biohackers. The study simply shows that ghrelin‑related compounds can affect pancreatic cell signaling, hinting that long‑term use of ghrelin‑boosting supplements might influence pancreas function, but more human research is needed before any actionable steps.
Summary
The researchers found that a type of pancreatic cell (AR42J) makes its own ghrelin and has ghrelin receptors. When ghrelin or a related peptide (GHRP‑6) is added, the cells show a two‑step rise in internal calcium, which can be blocked by specific inhibitors. This suggests the ghrelin system plays a role in how the exocrine pancreas works.
Abstract
Ghrelin is an endogenous ligand for the growth hormone secretagogue receptor. The presence of ghrelin in pancreatic islet cells has been previously reported and it is known to increase the [Ca2+]i in (-cells, affecting insulin secretion. However, evidence for the existence of the ghrelin system and its calcium signalling pathway in the exocrine pancreas remains unclear. Thus this study aims, first, to investigate the expression of ghrelin and its receptor in pancreatic AR42J cells and, secondly, to elucidate its calcium signalling pathway. Our results showed that ghrelin and ghrelin receptor were consistently expressed in AR42J cells. Moreover, fluorescence imaging showed that cholecystokinin-8, ghrelin and growth hormone-releasing hexapeptide stimulate [Ca2+]i in AR42J cells in a dose-dependent manner. Ghrelin and the hexapeptide produced a biphasic elevation in [Ca2+]i with an initial transient increase, followed by a sustained plateau. In the presence of (D-Lys3)-GHRP-6, the [Ca2+]i evoked by ghrelin was suppressed. In the absence of extracellular Ca2+, the transient phase of the ghrelin response was maintained but greatly diminished while the plateau phase was completely abolished. Pretreatment with 2-aminoethoxydiphenyl borate and xestospongin C abolished the transient phase and inhibited the sustained phase of the ghrelin response. The stimulatory effect of ghrelin was also blocked by nifedipine. These results indicate that ligand stimulation of the ghrelin receptor could lead to a biphasic [Ca2+]i mobilization in these cells. These data suggests the presence of a ghrelin system in pancreatic AR42J cells. In addition, its roles in exocrine function are implicated in the pancreas.
Study Information
pubmed
2005
10.1016/j.biocel.2004.11.012