title: Enhanced gastric emptying of a liquid gastric load in mice lacking cholecystokinin-B receptor: a study of CCK-A,B, and AB receptor gene knockout mice.
abstract: BACKGROUND
  Although cholecystokinin (CCK) has been shown to inhibit gastric emptying via CCK-A receptors (CCK-ARs), the role of CCK-B receptors (CCK-BRs) has not been verified. We examined whether gastric emptying of a nonnutrient liquid load was modified in CCK-AR, BR, and ARBR gene knockout mice.
  
  
  METHODS
  A liquid gastric load prepared with phenol red was administered via an orogastric tube (0.15 ml/mouse). The animals were killed by decapitation, and gastric emptying was estimated at 10 and 30 min after ingestion. The effects of the sulfated form of CCK-8 (CCK-8S) and of graded doses of atropine were examined. In addition, a proton pump inhibitor was administered to wild-type mice to examine the contribution of gastric acid to emptying.
  
  
  RESULTS
  Gastric emptying was significantly enhanced in mice lacking CCK-BR, as compared with wild-type and CCK-AR(-/-) mice. CCK-8S inhibited gastric emptying in mice with CCK-AR, but not in mice without CCK-AR. A proton pump inhibitor did not affect gastric emptying. Atropine dose dependently inhibited gastric emptying in all genotypes. The thickness of smooth muscle was comparable for all genotypes.
  
  
  CONCLUSIONS
  The gastric emptying of a nonnutrient liquid load was enhanced in mice without CCK-BR, although the precise mechanism is not known. Although cholecystokinin (CCK) has been shown to inhibit gastric emptying via CCK-A receptors (CCK-ARs), the role of CCK-B receptors (CCK-BRs) has not been verified. We examined whether gastric emptying of a nonnutrient liquid load was modified in CCK-AR, BR, and ARBR gene knockout mice.
authors.affiliation: Department of Clinical Physiology, Tokyo Metropolitan Institute of Gerontology, 35-2 Sakaecho, Itabashi-ku, Tokyo, 173-0015, Japan.
authors.forename: Kyoko
authors.initials: K
authors.lastname: Miyasaka
authors.forename: Minoru
authors.initials: M
authors.lastname: Ohta
authors.forename: Setsuko
authors.initials: S
authors.lastname: Kanai
authors.forename: Yuki
authors.initials: Y
authors.lastname: Yoshida
authors.forename: Norikazu
authors.initials: N
authors.lastname: Sato
authors.forename: Aki
authors.initials: A
authors.lastname: Nagata
authors.forename: Toshimitsu
authors.initials: T
authors.lastname: Matsui
authors.forename: Tetsuo
authors.initials: T
authors.lastname: Noda
authors.forename: Atsuo
authors.initials: A
authors.lastname: Jimi
authors.forename: Soichi
authors.initials: S
authors.lastname: Takiguchi
authors.forename: Yutaka
authors.initials: Y
authors.lastname: Takata
authors.forename: Takako
authors.initials: T
authors.lastname: Kawanami
authors.forename: Akihiro
authors.initials: A
authors.lastname: Funakoshi
mesh_terms: D000818:Animals; D004791:Enzyme Inhibitors / Q000494:pharmacology; D005746:Gastric Emptying / Q000187:drug effects / Q000502:physiology*; D008297:Male; D051379:Mice; D018345:Mice, Knockout; D023421:Models, Animal; D009853:Omeprazole / Q000494:pharmacology; D054328:Proton Pump Inhibitors; D043887:Receptor, Cholecystokinin B / Q000187:drug effects / Q000235:genetics / Q000502:physiology*
chemical_list: D004791:Enzyme Inhibitors; D054328:Proton Pump Inhibitors; D043887:Receptor, Cholecystokinin B; D009853:Omeprazole