title: Interdigestive migrating motor complex -its mechanism and clinical importance.
abstract: Migrating motor complex (MMC) is well characterized by the appearance of gastrointestinal (GI) contractions in the interdigestive state. The physiological importance of gastric MMC is a mechanical and chemical cleansing of the empty stomach in preparation for the next meal. MMC cycle is mediated via the interaction between motilin and 5-hydroxytryptamine (5-HT) by the positive feedback mechanism in conscious dogs. Luminal administration of 5-HT initiates duodenal phase II and phase III with a concomitant increase of plasma motilin release. Duodenal 5-HT concentration is increased during gastric phase II and phase III. Intravenous infusion of motilin increases luminal 5-HT content and induces phase III. 5-HT4 antagonists significantly inhibit both of gastric and intestinal phase III, while 5-HT3 antagonists inhibit only gastric phase III. These suggest that gastric MMC is regulated via vagus, 5-HT3/4 receptors and motilin, while intestinal MMC is regulated via intrinsic primary afferent neurons (IPAN) and 5-HT4 receptors. We propose the possibility that maximally released motilin by a positive feedback depletes 5-HT granules in the duodenal EC cells, resulting in no more contractions. Stress is highly associated with the pathogenesis of functional dyspepsia (FD). Acoustic stress attenuates gastric phase III without affecting intestinal phase III in conscious dogs, via reduced vagal activity. Subset of FD patients shows reduced vagal activity and impaired gastric phase III. The impaired gastric MMC may aggravate dyspeptic symptoms following a food ingestion. Maintaining MMC cycle in the interdigestive state is an important factor to prevent the postprandial dyspeptic symptoms.
authors.affiliation: Department of Surgery and Department of Neurology, Medical College of Wisconsin and Zablocki VA Medical Center, Milwaukee, Wisconsin, USA.
authors.forename: Toku
authors.initials: T
authors.lastname: Takahashi
mesh_terms: D000818:Animals; D004063:Digestion / Q000187:drug effects / Q000502:physiology*; D004285:Dogs; D004386:Duodenum / Q000378:metabolism; D004415:Dyspepsia / Q000209:etiology* / Q000517:prevention & control*; D025461:Feedback, Physiological / Q000502:physiology; D005746:Gastric Emptying / Q000502:physiology; D006801:Humans; D007422:Intestines / Q000502:physiology; D009037:Motilin / Q000008:administration & dosage / Q000097:blood / Q000502:physiology; D016065:Myoelectric Complex, Migrating / Q000502:physiology*; D009475:Neurons, Afferent / Q000502:physiology; D019518:Postprandial Period; D044406:Receptors, Serotonin, 5-HT3 / Q000502:physiology; D044422:Receptors, Serotonin, 5-HT4 / Q000502:physiology; D012701:Serotonin / Q000008:administration & dosage / Q000378:metabolism / Q000502:physiology; D058831:Serotonin 5-HT3 Receptor Antagonists / Q000494:pharmacology; D058832:Serotonin 5-HT4 Receptor Antagonists / Q000494:pharmacology; D013270:Stomach / Q000502:physiology*; D014630:Vagus Nerve / Q000502:physiology
chemical_list: D044406:Receptors, Serotonin, 5-HT3; D058831:Serotonin 5-HT3 Receptor Antagonists; D058832:Serotonin 5-HT4 Receptor Antagonists; D044422:Receptors, Serotonin, 5-HT4; D012701:Serotonin; D009037:Motilin