Abstract
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. D cells were quantified by morphometry and flow cytometry in 16-wk-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 them with omeprazole for 2 mo. G-/- mice showed significant inflammation compared with the G+/+ mice, which resolved after 20 days of antibiotic treatment. D cell numbers were not significantly different between G-/- and G+/+ mice. After G-17 was infused, fundic and antral D cell numbers decreased in the G-/- mice. G+/+ animals made hypergas-trinemic 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. 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.
Original language | English (US) |
---|---|
Pages (from-to) | G175-G183 |
Journal | American Journal of Physiology - Gastrointestinal and Liver Physiology |
Volume | 282 |
Issue number | 1 45-1 |
DOIs | |
State | Published - 2002 |
Externally published | Yes |
Keywords
- Bacterial overgrowth
- Gastrin-null mice
- Helicobacter pylori
- Mucosal lymphocytes
- Omeprazole
ASJC Scopus subject areas
- Physiology
- Hepatology
- Gastroenterology
- Physiology (medical)