Impaired gastric acid secretion in gastrin-deficient mice
Research output: Contribution to journal › Journal article › Research › peer-review
Standard
Impaired gastric acid secretion in gastrin-deficient mice. / Friis-Hansen, Lennart; Sundler, Frank; Li, Ying; Gillespie, Patrick J.; Saunders, Thomas L.; Greenson, Joel K.; Owyang, Chung; Rehfeld, Jens F.; Samuelson, Linda C.
In: American Journal of Physiology - Gastrointestinal and Liver Physiology, Vol. 274, No. 3 37-3, 03.1998, p. G561-G568.Research output: Contribution to journal › Journal article › Research › peer-review
Harvard
APA
Vancouver
Author
Bibtex
}
RIS
TY - JOUR
T1 - Impaired gastric acid secretion in gastrin-deficient mice
AU - Friis-Hansen, Lennart
AU - Sundler, Frank
AU - Li, Ying
AU - Gillespie, Patrick J.
AU - Saunders, Thomas L.
AU - Greenson, Joel K.
AU - Owyang, Chung
AU - Rehfeld, Jens F.
AU - Samuelson, Linda C.
PY - 1998/3
Y1 - 1998/3
N2 - To further understand the role of the peptide hormone gastrin in the development and function of the stomach, we have generated gastrin-deficient mice by gene targeting in embryonic stem cells. Mutant mice were viable and fertile, without obvious visible abnormalities. However, gastric function was severely affected by the loss of gastrin. Basal gastric acid secretion was abolished and could not be induced by histamine, carbachol, or gastrin. Histological analysis revealed alterations in the two cell types primarily involved in acid secretion, parietal and enterochromaffin-like (ECL) cells. Parietal cells were reduced in number with an accumulation of immature cells lacking H+-K+-adenosinetriphosphatase (H+-K+-ATPase). ECL cells were positioned closer to the base of the gastric glands, with markedly lower expression of histidine decarboxylase. Gastrin administration for 6 days reversed the effects of the gastrin deficiency, leading to an increase in the number of mature, H+-K+-ATPase-positive parietal cells and a partial restoration of acid secretion. The results show that gastrin is critically important for the function of the acid secretory system.
AB - To further understand the role of the peptide hormone gastrin in the development and function of the stomach, we have generated gastrin-deficient mice by gene targeting in embryonic stem cells. Mutant mice were viable and fertile, without obvious visible abnormalities. However, gastric function was severely affected by the loss of gastrin. Basal gastric acid secretion was abolished and could not be induced by histamine, carbachol, or gastrin. Histological analysis revealed alterations in the two cell types primarily involved in acid secretion, parietal and enterochromaffin-like (ECL) cells. Parietal cells were reduced in number with an accumulation of immature cells lacking H+-K+-adenosinetriphosphatase (H+-K+-ATPase). ECL cells were positioned closer to the base of the gastric glands, with markedly lower expression of histidine decarboxylase. Gastrin administration for 6 days reversed the effects of the gastrin deficiency, leading to an increase in the number of mature, H+-K+-ATPase-positive parietal cells and a partial restoration of acid secretion. The results show that gastrin is critically important for the function of the acid secretory system.
KW - Achlorhydria
KW - Gastric mucosa
KW - Gastrointestinal hormones
KW - Knockout mice
KW - Parietal cells
UR - http://www.scopus.com/inward/record.url?scp=0031948701&partnerID=8YFLogxK
U2 - 10.1152/ajpgi.1998.274.3.g561
DO - 10.1152/ajpgi.1998.274.3.g561
M3 - Journal article
C2 - 9530158
AN - SCOPUS:0031948701
VL - 274
SP - G561-G568
JO - American Journal of Physiology: Gastrointestinal and Liver Physiology
JF - American Journal of Physiology: Gastrointestinal and Liver Physiology
SN - 0193-1857
IS - 3 37-3
ER -
ID: 310767623