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Gastrointestinal motility modulation via gut hormone regulation is a physiological process involving the release of signaling peptides from enteroendocrine cells to coordinate the movement of the digestive tract. This mechanism relies on the activation of specific G protein-coupled receptors (GPCRs), including the Glucagon-like peptide-1 receptor (GLP-1R), the Ghrelin receptor (GHSR), and the Motilin receptor (MLNR) [Source: PubMed, PMID: 17209178]. Hormones such as GLP-1 and Cholecystokinin (CCK) function to slow gastric emptying and intestinal transit, a process often referred to as the "ileal brake" [Source: StatPearls, NBK551568]. In contrast, Ghrelin and Motilin act as prokinetic signals that stimulate gastric contractions and the migrating motor complex [Source: NIH, PMC2654796]. This regulatory network is a major therapeutic target for disorders like gastroparesis, where prokinetic agonists are employed to enhance motility [Source: PubMed, PMID: 29330230]. It is also central to the management of Type 2 diabetes and obesity, where GLP-1 receptor agonists are used to delay gastric emptying and promote satiety [Source: PubMed, PMID: 21864752]. Dysregulation of these hormonal pathways can lead to functional gastrointestinal disorders, including irritable bowel syndrome and chronic constipation. Drugs targeting these receptors must balance efficacy in motility with potential side effects such as nausea, vomiting, and glycemic fluctuations.
Modulation of gastrointestinal transit through the agonism or antagonism of gut-derived hormone receptors (e.g., GLP-1R, GHSR, MLNR) to alter smooth muscle contractility and enteric nervous system activity.
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