Altered control of gastric acid secretion in gastrin-cholecystokinin double mutant mice

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Altered control of gastric acid secretion in gastrin-cholecystokinin double mutant mice. / Chen, D; Zhao, CM; Håkanson, Rolf; Samuelson, LC; Rehfeld, JF; Friis-Hansen, L.

I: Gastroenterology, Vol. 126, Nr. 2, 2004, s. 476-487.

Forskningsoutput: TidskriftsbidragArtikel i vetenskaplig tidskrift

Harvard

Chen, D, Zhao, CM, Håkanson, R, Samuelson, LC, Rehfeld, JF & Friis-Hansen, L 2004, 'Altered control of gastric acid secretion in gastrin-cholecystokinin double mutant mice', Gastroenterology, vol. 126, nr. 2, s. 476-487. https://doi.org/10.1053/j.gastro.2003.11.012

APA

Chen, D., Zhao, CM., Håkanson, R., Samuelson, LC., Rehfeld, JF., & Friis-Hansen, L. (2004). Altered control of gastric acid secretion in gastrin-cholecystokinin double mutant mice. Gastroenterology, 126(2), 476-487. https://doi.org/10.1053/j.gastro.2003.11.012

CBE

Chen D, Zhao CM, Håkanson R, Samuelson LC, Rehfeld JF, Friis-Hansen L. 2004. Altered control of gastric acid secretion in gastrin-cholecystokinin double mutant mice. Gastroenterology. 126(2):476-487. https://doi.org/10.1053/j.gastro.2003.11.012

MLA

Vancouver

Author

Chen, D ; Zhao, CM ; Håkanson, Rolf ; Samuelson, LC ; Rehfeld, JF ; Friis-Hansen, L. / Altered control of gastric acid secretion in gastrin-cholecystokinin double mutant mice. I: Gastroenterology. 2004 ; Vol. 126, Nr. 2. s. 476-487.

RIS

TY - JOUR

T1 - Altered control of gastric acid secretion in gastrin-cholecystokinin double mutant mice

AU - Chen, D

AU - Zhao, CM

AU - Håkanson, Rolf

AU - Samuelson, LC

AU - Rehfeld, JF

AU - Friis-Hansen, L

PY - 2004

Y1 - 2004

N2 - Background & Aims: Three pathways control gastric acid secretion: the gastrin-enterochromaffin-like (ECL) cell axis, the vagus-parietal cell axis, and the cholecystokinin (CCK)-D cell axis. Mice lacking gastrin or both gastrin and CCK were examined to determine the role of the hormones. Methods: Acid was measured after pylorus ligation, and biopsies from gastrin knockout (KO), gastrin-CCK double-KO, and wild-type (WT) mice were collected for biochemical, immunocytochemical, and electron-microscopic examination. Results: The ECL cells were inactive in both groups of mutant mice but the cell number was unaffected. Both parietal cell number and level of H+/K+-ATPase messenger RNA (mRNA) were reduced in the mutant strains, but gastrin-CCK double-KO mice displayed more active parietal cells and larger acid output than the gastrin KO mice. The acid response to histamine in double-KO mice was unchanged whereas that to gastrin was diminished, but it could be restored by infusion of gastrin. Oxyntic D-cell density was the same in both mutant strains, but the D cells were more active in the gastrin KO than in the double-KO mice. CCK infusion in gastrin-CCK double-KO mice raised the somatostatin mRNA level and inhibited acid secretion to the level seen in gastrin KO mice. Vagotomy and atropine abolished acid secretion in all 3 groups of mice. Conclusions: Lack of gastrin impairs the gastrin-ECL axis, whereas lack of gastrin and CCK impairs both hormonal pathways. In the gastrin-CCK double-KO mice, acid secretion is only controlled by cholinergic vagal stimulation, which normalizes the acid output.

AB - Background & Aims: Three pathways control gastric acid secretion: the gastrin-enterochromaffin-like (ECL) cell axis, the vagus-parietal cell axis, and the cholecystokinin (CCK)-D cell axis. Mice lacking gastrin or both gastrin and CCK were examined to determine the role of the hormones. Methods: Acid was measured after pylorus ligation, and biopsies from gastrin knockout (KO), gastrin-CCK double-KO, and wild-type (WT) mice were collected for biochemical, immunocytochemical, and electron-microscopic examination. Results: The ECL cells were inactive in both groups of mutant mice but the cell number was unaffected. Both parietal cell number and level of H+/K+-ATPase messenger RNA (mRNA) were reduced in the mutant strains, but gastrin-CCK double-KO mice displayed more active parietal cells and larger acid output than the gastrin KO mice. The acid response to histamine in double-KO mice was unchanged whereas that to gastrin was diminished, but it could be restored by infusion of gastrin. Oxyntic D-cell density was the same in both mutant strains, but the D cells were more active in the gastrin KO than in the double-KO mice. CCK infusion in gastrin-CCK double-KO mice raised the somatostatin mRNA level and inhibited acid secretion to the level seen in gastrin KO mice. Vagotomy and atropine abolished acid secretion in all 3 groups of mice. Conclusions: Lack of gastrin impairs the gastrin-ECL axis, whereas lack of gastrin and CCK impairs both hormonal pathways. In the gastrin-CCK double-KO mice, acid secretion is only controlled by cholinergic vagal stimulation, which normalizes the acid output.

U2 - 10.1053/j.gastro.2003.11.012

DO - 10.1053/j.gastro.2003.11.012

M3 - Article

VL - 126

SP - 476

EP - 487

JO - Gastroenterology

JF - Gastroenterology

SN - 1528-0012

IS - 2

ER -