Abstract
In structure, ghrelin resembles motilin. The two peptides are considered to be members of the motilin-ghrelin peptide family. Motilin is considered to be an endocrine regulator of the interdigestive migrating contractions, the fasted motor pattern in the gastrointestinal (GI) tract. It has been reported that ghrelin stimulates GI motility. The gastrokinetic capacity of ghrelin has been well documented in the rodent. However, there have been few positive reports of the gastrokinetic capacity of ghrelin in dogs. Some reports with human subjects have shown that an i.v. ghrelin injection accelerated gastric emptying of a meal and improved meal-related symptoms. These results suggest that ghrelin has potential as a prokinetic. However, it seems unlikely that plasma ghrelin would play a physiological role in these digestive physiological events and stimulate gastric emptying, as these outcomes would appear to be in contradiction with the suppression of the endogenous release of ghrelin after eating. The physiological roles of ghrelin need to be clarified.
Highlights
Ghrelin is a 28-amino-acid peptide predominantly produced by endocrine cells in the oxyntic mucosa of the stomach as an endogenous ligand for the growth hormone (GH) secretagogue receptor [1,2,3,4]
This review focuses on the capacity of ghrelin to act on GI motility and compares the findings with those of motilin mainly in the dog
This notion is supported by a study by Peeters et al [34], who described phase III motor activities starting in the stomach or the upper duodenum that are associated with plasma motilin peaks, and another by Lee et al [35], who reported that immunoneutralization of circulating motilin suppresses phase III contractions
Summary
Ghrelin is a 28-amino-acid peptide predominantly produced by endocrine cells in the oxyntic mucosa of the stomach as an endogenous ligand for the growth hormone (GH) secretagogue receptor [1,2,3,4]. Motilin plasma levels increase cyclically every 90–120 minutes during the interdigestive fasting period, and this cyclical release of motilin disappears after ingestion of a meal These cyclical peaks of plasma motilin are synchronized to strong peristaltic contractions initiated from the stomach and migrating to the duodenum and small intestine. Ghrelin induces premature phase III contractions of IMC in the human stomach [21]. Endogenous ghrelin has been reported to be involved in mediating phase III-like contractions in the stomach of rats [26] and mice [27]. Itoh et al [36] found that the effect of motilin on phase III activity in dogs was blocked by a 5-hydroxytryptamine-3 (5-HT3) antagonist This finding suggests that the motilininduced signal may be mediated via 5-HT3 receptors on the vagal afferents. This review focuses on the capacity of ghrelin to act on GI motility and compares the findings with those of motilin mainly in the dog
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