Effect of cholecystokinin on gastric motility in humans.
Gastric emptying after food ingestion is regulated by neural and hormonal factors. However, the relative contributions of each pathway is not yet clearly defined. The classic gut hormone CCK seems to be involved in the regulation of gastric emptying in humans. Experimental evidence is best for gastric emptying of liquid meals that release CCK from the duodenum: (1) CCK infused at postprandial plasma concentrations inhibits gastric emptying of a liquid and a semisolid meal. (2) Administration of the CCK antagonist loxiglumide significantly accelerated gastric emptying of a liquid mixed meal and a glucose meal. Discrepant results with the antagonist MK329 are difficult to explain considering the marked acceleration of gastric emptying rates by the specific and potent antagonist MK329 shown in several animal studies. Taken together, current information favors the conclusion, however, that CCK mainly controls gastric emptying of the liquid but not the solid components. Thus, CCK is involved in the physiologic regulation of gastric emptying and gastric motility in man. Blocking CCK-A receptors accelerates gastric emptying of liquid meals and abolishes the gastrocolonic reflex. Therefore, CCK may play a role as a common regulator of postprandial gallbladder contraction and pancreatic enzyme secretion as well as of gastric emptying rates under certain conditions. Such common control would optimize the nutrient-to-digestive juices concentration ratio. The importance of endogenous CCK on gastric emptying of solid meals, however, is poorly understood and remains to be defined. Only very limited information is available on gastric motility. Much more work has to be done before a clear concept can be developed.
Beglinger
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Division of Gastroenterology, University Hospital, Basel, Switzerland.
D001570:Benzodiazepinones / Q000494:pharmacology; D002766:Cholecystokinin / Q000008:administration & dosage / Q000494:pharmacology*; D003106:Colon / Q000187:drug effects / Q000502:physiology; D020109:Devazepide; D004064:Digestive System / Q000187:drug effects; D004068:Digestive System Physiological Phenomena; D004386:Duodenum / Q000187:drug effects / Q000502:physiology; D005746:Gastric Emptying / Q000187:drug effects*; D005769:Gastrointestinal Motility / Q000187:drug effects*; D006801:Humans; D007082:Ileum / Q000187:drug effects / Q000502:physiology; D007262:Infusions, Intravenous; D011377:Proglumide / Q000031:analogs & derivatives / Q000494:pharmacology; D011949:Receptors, Cholecystokinin / Q000037:antagonists & inhibitors / Q000502:physiology; D012844:Sincalide / Q000494:pharmacology
D001570:Benzodiazepinones; D011949:Receptors, Cholecystokinin; C053737:loxiglumide; D002766:Cholecystokinin; D011377:Proglumide; D020109:Devazepide; D012844:Sincalide