Literature DB >> 1150048

Radioautographic and quantitative studies on parietal and peptic cell kinetics in the mouse. A selective effect of gastrin on parietal cell proliferation.

G Willems, T Lehy.   

Abstract

Gastrin was given to mice subcutaneously at 8-hr intervals for 20 days. Control animals received only saline injections. With use of [3H]thymidine and radioautography, a significant increase in the production of new parietal cells (P less than 0.01) was observed in the gastrin-treated group. Increases in fundic progenitor cell DNA synthesis and shortened maturation time of the latter were demonstrated. Both could explain the observed changes in parietal cell kinetics. The quantitative estimation of parietal cell population after the administration of gastrin showed an increase in average parietal cell count per unit (P less than 0.01) and in total parietal cell number (P less than 0.05). This was consistent with the observed acceleration in the rate of parietal cell production under influence of gastrin. In contrast, no radioautographic difference in the proliferative activity of the peptic cells was observed between the gastrin-treated and the control mice. Moreover, at the end of the experiment, no changes in average peptic cell count per unit area, or in total peptic cell number, occurred under the effect of gastrin. The observation that peptic cells are renewed in a different way, independently from fundic progenitor cells and from parietal cells, was consistent with their peculiar lack in proliferative response to the hormone.

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Year:  1975        PMID: 1150048

Source DB:  PubMed          Journal:  Gastroenterology        ISSN: 0016-5085            Impact factor:   22.682


  14 in total

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8.  Administration of caerulein to rats promotes antral epithelial cell renewal.

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9.  Eradicating Helicobacter pylori infection lowers gastrin mediated acid secretion by two thirds in patients with duodenal ulcer.

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10.  Proliferation and Differentiation of Gastric Mucous Neck and Chief Cells During Homeostasis and Injury-induced Metaplasia.

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