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Am J Physiol Gastrointest Liver Physiol 277: G500-G505, 1999;
0193-1857/99 $5.00
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Vol. 277, Issue 3, G500-G505, September 1999

THEMES
Lessons From Genetically Engineered Animal Models
III. Lessons learned from gastrin gene deletion in mice*

Karen L. Hinkle and Linda C. Samuelson

Department of Physiology, The University of Michigan, Ann Arbor, Michigan 48109-0622

Gastrin is the principal hormonal inducer of gastric acid secretion. Chronic hypergastrinemia, leading to hypersecretion of gastric acid and increased proliferation of parietal and enterochromaffin-like (ECL) cells, has been well described. In contrast, the physiological consequences of chronic gastrin deficiency had been poorly understood until the recent genetic engineering of mouse mutants containing a gastrin gene deletion by homologous recombination in embryonic stem cells. This themes article describes the consequences of constitutive gastrin deficiency on the development and physiology of the stomach. A lack of gastrin disrupts basal gastric acid secretion and renders the acid secretory system unresponsive to acute histaminergic, cholinergic, and gastrinergic stimulation. The defect in acid secretion is greater than would have been predicted from previous studies in which gastrin action was acutely blocked. Cellular changes include thinning of the gastric mucosa in the gastrin-deficient mice, with a reduction in parietal cells and reduced expression of markers of parietal and ECL cell-differentiated functions. The results suggest that gastrin is required for the functional maturation of the acid-secretory system.

hypochlorhydria; gastrointestinal hormones; knockout mice; parietal cells; enterochromaffin-like cells

* Third in a series of invited articles on Lessons From Genetically Engineered Animal Models.




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