Hypergastrinemia in response to gastric inflammation suppresses somatostatin.

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 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. 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.

• Authors: Yana Zavros, Gabriele Rieder, Amy Ferguson, Linda C Samuelson, Juanita L Merchant
• Journal: American journal of physiology. Gastrointestinal and liver physiology (Am J Physiol Gastrointest Liver Physiol) Vol. 282 Issue 1 Pg. G175-83 (Jan 2002) ISSN: 0193-1857 [Print] United States
• PMID: 11751171 (Publication Type: Journal Article, Research Support, U.S. Gov't, P.H.S.)

Chemical References

• Anti-Ulcer Agents
• Gastrins
• Somatostatin
• gastrin 17
• Omeprazole

Topics

• Animals
• Anti-Ulcer Agents (pharmacology)
• Female
• Gastric Acid (metabolism)
• Gastric Fundus (cytology, immunology, microbiology)
• Gastric Mucosa (cytology, immunology)
• Gastrins (blood, genetics, pharmacology)
• Gastritis (metabolism, microbiology, physiopathology)
• Helicobacter Infections (metabolism, physiopathology)
• Helicobacter pylori
• Lymphocytes (physiology)
• Male
• Mice
• Mice, Inbred C57BL
• Mice, Knockout
• Omeprazole (pharmacology)
• Parietal Cells, Gastric (cytology, immunology, metabolism)
• Pyloric Antrum (cytology, immunology, microbiology)
• Somatostatin (metabolism)