Impaired gastric acid secretion in gastrin-deficient mice

Research output: Journal Publications and ReviewsRGC 21 - Publication in refereed journalpeer-review

199 Scopus Citations
View graph of relations

Author(s)

  • Lennart Friis-Hansen
  • Frank Sundler
  • Patrick J. Gillespie
  • Thomas L. Saunders
  • Joel K. Greenson
  • Chung Owyang
  • Jens F. Rehfeld
  • Linda C. Samuelson

Detail(s)

Original languageEnglish
Pages (from-to)G561-G568
Journal / PublicationAmerican Journal of Physiology - Gastrointestinal and Liver Physiology
Volume274
Issue number3
Publication statusPublished - Mar 1998
Externally publishedYes

Abstract

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.

Research Area(s)

  • Achlorhydria, Gastric mucosa, Gastrointestinal hormones, Knockout mice, Parietal cells

Citation Format(s)

Impaired gastric acid secretion in gastrin-deficient mice. / Friis-Hansen, Lennart; Sundler, Frank; Li, Ying et al.
In: American Journal of Physiology - Gastrointestinal and Liver Physiology, Vol. 274, No. 3, 03.1998, p. G561-G568.

Research output: Journal Publications and ReviewsRGC 21 - Publication in refereed journalpeer-review