GHRP-6
Growth Hormone Releasing Peptide-6, Growth hormone-releasing hexapeptide, His-D-Trp-Ala-Trp-D-Phe-Lys-NH2
Ghrelin suppresses cholecystokinin (CCK), peptide YY (PYY) and glucagon-like peptide-1 (GLP-1) in the intestine, and attenuates the anorectic effects of CCK, PYY and GLP-1 in goldfish (Carassius auratus).
Blanco. Ayelén Melisa AM; Bertucci. Juan Ignacio JI; Valenciano. Ana Isabel AI; Delgado. María Jesús MJ; Unniappan. Suraj S
Key Findings
- Ghrelin and its receptor GHS‑R1a are colocalized with CCK, PYY and GLP‑1 cells in the intestinal lining
- Ghrelin exposure lowers the gene and protein expression of CCK, PYY and GLP‑1 in intestinal explants, an effect blocked by a GHS‑R1a antagonist
- Co‑administration of ghrelin with CCK, PYY or GLP‑1 does not change food intake, indicating ghrelin overrides their anorectic effects
Practical Outcomes
- For biohackers, this hints that ghrelin‑mimicking peptides like GHRP‑6 might dampen the body’s satiety signals and boost appetite, but the data come from goldfish and may not translate directly to humans. Until human studies confirm this, any protocol changes should be cautious and based on broader evidence.
Summary
In goldfish, the hunger hormone ghrelin (and its receptor) sits right next to cells that make the fullness hormones CCK, PYY, and GLP‑1. When ghrelin is added, the fish’s gut makes less of those satiety hormones, and this drop is stopped if a ghrelin‑blocker is used. Even when the satiety hormones are given together with ghrelin, the fish still eats the same amount, meaning ghrelin overpowers their appetite‑reducing signals. This shows ghrelin can suppress the body’s natural “stop‑eating” signals, at least in fish.
Abstract
Ghrelin is an important gut-derived hormone with an appetite stimulatory role, while most of the intestinal hormones, including cholecystokinin (CCK), peptide YY (PYY) and glucagon-like peptide-1 (GLP-1), are appetite-inhibitors. Whether these important peptides with opposing roles on food intake interact to regulate energy balance in fish is currently unknown. The aim of this study was to characterize the putative crosstalk between ghrelin and CCK, PYY and GLP-1 in goldfish (Carassius auratus). We first determined the localization of CCK, PYY and GLP-1 in relation to ghrelin and its main receptor GHS-R1a (growth hormone secretagogue 1a) in the goldfish intestine by immunohistochemistry. Colocalization of ghrelin/GHS-R1a and CCK/PYY/GLP-1 was found primarily in the luminal border of the intestinal mucosa. In an intestinal explant culture, a significant decrease in prepro-cck, prepro-pyy and proglucagon transcript levels was observed after 60min of incubation with ghrelin, which was abolished by preincubation with the GHS-R1a ghrelin receptor antagonist [D-Lys3]-GHRP-6 (except for proglucagon). The protein expression of PYY and GLP-1 was also downregulated by ghrelin. Finally, intraperitoneal co-administration of CCK, PYY or GLP-1 with ghrelin results in no modification of food intake in goldfish. Overall, results of the present study show for the first time in fish that ghrelin exerts repressive effects on enteric anorexigens. It is likely that these interactions mediate the stimulatory effects of ghrelin on feeding and metabolism in fish.
Study Information
pubmed
2017
2017-05-18T00:00:00.000Z
10.1016/j.yhbeh.2017.05.004
30
53