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Articles in PresS, published online ahead of print October 15, 2001
Am J Physiol Gastrointest Liver Physiol, 10.1152/ajpgi.00287.2001
Submitted on July 3, 2001
Accepted on September 21, 2001
1 Howard Hughes Medical Institute, Ann Arbor, MI, USA
2 Internal Medicine, University of Michigan, Ann Arbor, MI, USA
3 Pathology, Univeristy of Michigan, Ann Arbor, MI, USA
4 Physiology, University of Michigan, Ann Arbor, MI, USA; Physiology, University of Michigan, Ann Arbor, MI, USA; Physiology, University of Michigan, Ann Arbor, MI, USA
5 Howard Hughes Medical Institute, Ann Arbor, MI, USA; Internal Medicine, University of Michigan, Ann Arbor, MI, USA; Physiology, University of Michigan, Ann Arbor, MI, USA
* To whom correspondence should be addressed. E-mail: merchanj{at}umich.edu.
Background: Hypergastrinemia and a reduction in tissue somatostatin occur in Helicobacter pylori-infected patients. We investigated whether the D cell may be a direct target of gastric inflammation and hypergastrinemia. Methods: D cells were quantified by morphometry and flow cytometry in 16 week old wild type (G+/+) and gastrin-deficient (G-/-) mice. Hypochlorhydric G-/- mice were treated with either antibiotics for 20 days or infused with gastrin (G-17) for 14 days. G+/+ mice were made hypochlorhydric by treating mice with omeprazole for 2 months. Results: G-/- mice showed significant inflammation when compared to the G+/+ mice which resolved after 20 days of antibiotic treatment. D cell numbers were not significantly different between G-/- and G+/+ mice. After infusing G-17, fundic and antral D cell numbers decreased in the G-/- mice. G+/+ animals made hypergastrinemic with omeprazole exhibited decreased D cell numbers. When omeprazole treated mice were treated with antibiotics alone, elevated plasma gastrin levels returned to baseline and D cell numbers returned to resting levels despite persistent hypochlorhydria. Conclusion: Hypergastrinemia, induced by inflammation, results in decreased D cell numbers. Thus, the stomach responds to the presence of inflammation by reducing somatostatin levels thereby releasing the inhibition on the G and parietal cells to maximize gastric acid output.
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