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This chapter summarizes the anatomy of the small bowel and colon and the control of gastrointestinal motility. The small intestine comprises mucosa, submucosa, muscularis, and serosa; the myenteric (Auerbach) and submucosal (Meissner) plexuses, with interstitial cells of Cajal, coordinate circular and longitudinal muscle. In the colon, thickened longitudinal bands (teniae coli) form haustra. Motility patterns include peristalsis, segmentation for mixing, and the migrating motor complexMigrating motor complex (MMC) (MMC; phases I–IV), which originates in the stomach, traverses the small intestine every 90–120 minutes during fasting, and is replaced postprandially. Colonic function features haustrations, peristalsis, and meal-induced mass peristalsis that drives defecation via rectal distension and sacral–pudendal reflexes. Autonomic inputs modulate but do not generate these rhythms. Enteroendocrine peptides provide state-dependent control: motilin initiates gastric MMCMigrating motor complex (MMC) phase III; ghrelin stimulates appetite and MMC; somatostatin suppresses gastric activity yet can trigger small-intestinal phase III; 5-hydroxytryptamine accelerates MMC propagation. After feeding, cholecystokinin (CCK) (via vagal/CCK1 pathways), glucose-dependent insulinotropic polypeptide, glucagon-like peptide-1, and peptide YY slow upper gastrointestinal transit, coordinate pyloric function, and promote absorption. Stress pathways further tune motility: corticotropin-releasing factor (CRF or corticotropin-releasing hormone) acting on CRF-R2 inhibits gastric activity, whereas CRF-R1 enhances colonic motility. Together, enteric circuits, autonomic inputs, and peptides integrate the feeding state with propulsion and continence.

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Small Bowel and Colon: Anatomy, Physiology of Gastrointestinal Motility, Peptides

  • 章节

  • 发表日期：

    2026年

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  • Masatomo Ishioh

摘要

This chapter summarizes the anatomy of the small bowel and colon and the control of gastrointestinal motility. The small intestine comprises mucosa, submucosa, muscularis, and serosa; the myenteric (Auerbach) and submucosal (Meissner) plexuses, with interstitial cells of Cajal, coordinate circular and longitudinal muscle. In the colon, thickened longitudinal bands (teniae coli) form haustra. Motility patterns include peristalsis, segmentation for mixing, and the migrating motor complexMigrating motor complex (MMC) (MMC; phases I–IV), which originates in the stomach, traverses the small intestine every 90–120 minutes during fasting, and is replaced postprandially. Colonic function features haustrations, peristalsis, and meal-induced mass peristalsis that drives defecation via rectal distension and sacral–pudendal reflexes. Autonomic inputs modulate but do not generate these rhythms. Enteroendocrine peptides provide state-dependent control: motilin initiates gastric MMCMigrating motor complex (MMC) phase III; ghrelin stimulates appetite and MMC; somatostatin suppresses gastric activity yet can trigger small-intestinal phase III; 5-hydroxytryptamine accelerates MMC propagation. After feeding, cholecystokinin (CCK) (via vagal/CCK1 pathways), glucose-dependent insulinotropic polypeptide, glucagon-like peptide-1, and peptide YY slow upper gastrointestinal transit, coordinate pyloric function, and promote absorption. Stress pathways further tune motility: corticotropin-releasing factor (CRF or corticotropin-releasing hormone) acting on CRF-R2 inhibits gastric activity, whereas CRF-R1 enhances colonic motility. Together, enteric circuits, autonomic inputs, and peptides integrate the feeding state with propulsion and continence.