title: Disruption of cholecystokinin (CCK)-B receptor gene did not modify bile or pancreatic secretion or pancreatic growth: a study in CCK-B receptor gene knockout mice.
abstract: Pancreatic exocrine function and bile secretion were examined in cholecystokinin (CCK)-B receptor gene-targeted mice and compared among different genotypes [i.e., CCK-B receptor gene: (+/+), wild-type; (+/-), heterozygous; and (-/-), homozygous deficient]. The histology and protein concentrations in the pancreas also were examined. Amylase release from the dispersed acini was examined in vitro by using the various doses of CCK-8, carbachol, and secretin. In vivo, the bile and pancreatic juice were collected, and the concentrations of amylase and bile acid were measured in anesthetized mice. The responses to CCK (100 pmol/kg) or acetyl-beta-methylcholine (500 nmol/kg) were examined. In vitro studies showed that the maximal effective concentrations of CCK-8 (10(-l0) M), carbachol (10(-5) M), and secretin (5 x 10(-7) M) were comparable for all genotypes. Fluid, amylase, and bile acid outputs in vivo also were comparable for all genotypes. Pancreatic wet weight and protein concentrations were not significantly different, and no abnormal findings were observed on histologic examination in any genotype. These results indicated that the CCK-B receptor has no role in pancreatic growth, exocrine secretion, or bile secretion in adult mice.
authors.affiliation: Department of Clinical Physiology, Tokyo Metropolitan Institute of Gerontology, Japan. miyasaka@tmig.or.jp
authors.forename: K
authors.initials: K
authors.lastname: Miyasaka
authors.forename: H
authors.initials: H
authors.lastname: Shinozaki
authors.forename: S
authors.initials: S
authors.lastname: Suzuki
authors.forename: Y
authors.initials: Y
authors.lastname: Sato
authors.forename: S
authors.initials: S
authors.lastname: Kanai
authors.forename: M
authors.initials: M
authors.lastname: Masuda
authors.forename: A
authors.initials: A
authors.lastname: Jimi
authors.forename: A
authors.initials: A
authors.lastname: Nagata
authors.forename: T
authors.initials: T
authors.lastname: Matsui
authors.forename: T
authors.initials: T
authors.lastname: Noda
authors.forename: A
authors.initials: A
authors.lastname: Kono
authors.forename: A
authors.initials: A
authors.lastname: Funakoshi
mesh_terms: D000375:Aging / Q000502:physiology*; D000681:Amylases / Q000187:drug effects / Q000378:metabolism; D000818:Animals; D001646:Bile / Q000378:metabolism*; D002217:Carbachol / Q000494:pharmacology; D005260:Female; D006579:Heterozygote; D006720:Homozygote; D051379:Mice; D018345:Mice, Knockout; D009929:Organ Size; D010179:Pancreas / Q000166:cytology / Q000187:drug effects / Q000502:physiology*; D010189:Pancreatic Juice / Q000378:metabolism*; D043887:Receptor, Cholecystokinin B; D011949:Receptors, Cholecystokinin / Q000172:deficiency / Q000235:genetics / Q000502:physiology*; D012633:Secretin / Q000494:pharmacology; D012844:Sincalide / Q000494:pharmacology
chemical_list: D043887:Receptor, Cholecystokinin B; D011949:Receptors, Cholecystokinin; D012633:Secretin; D002217:Carbachol; D000681:Amylases; D012844:Sincalide