Ghrelin was recently identified as the first endogenous ligand for growth hormone secretagogue receptors (previously
known as orphan receptors). Two major molecular forms of ghrelin are found in the stomach and plasma: acyl
ghrelin with O-n-octanoylated serine at position 3 and des-acyl ghrelin. Interestingly, these distinct molecular forms play
contrasting roles in ingestive behavior, upper gastrointestinal motility, and gastric acid secretion. Acyl ghrelin stimulates
food intake both in fed and fasted rodents and induces adiposity, alleviates ingestive behavior, stimulates gastrointestinal
motor activity and gastric acid secretion, and accelerates gastric emptying in several species. In contrast, des-acyl ghrelin
has been demonstrated to disrupt gastric motility in rats and delay gastric emptying in mice and rats. Thus, acyl ghrelin is
a potent stimulator of ingestive behavior, gastrointestinal motility, and gastric acid secretion, whereas des-acyl ghrelin exerts
opposing effects on ingestive behavior and gastrointestinal motility but does not affect gastric acid secretion. Ghrelin
is expected to be used in various applications such as therapeutic strategies for obesity, anorexia, cachexia, and cardiovascular
disease in the clinical setting. In this article, we review the evidence on the roles of acyl ghrelin and des-acyl ghrelin
in the regulation of ingestive behavior, upper gastrointestinal motility, and gastric acid secretion in mammals; moreover,
we mention the effects of ghrelin on oral functions.
Keywords: Acyl ghrelin, des-acyl ghrelin, food intake, ingestive behavior, gastric acid secretion, gastrointestinal motility, oral functions, secretion, therapeutic strategies, hormone.
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