Hypergastrinemia in response to gastric inflammation suppresses somatostatin

Yana Zavros, Gabriele Rieder, A. M.Y. Ferguson, Linda C. Samuelson, Juanita L. Merchant

Research output: Contribution to journalArticlepeer-review

53 Scopus citations


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 languageEnglish (US)
Pages (from-to)G175-G183
JournalAmerican Journal of Physiology - Gastrointestinal and Liver Physiology
Issue number1 45-1
StatePublished - 2002
Externally publishedYes


  • Bacterial overgrowth
  • Gastrin-null mice
  • Helicobacter pylori
  • Mucosal lymphocytes
  • Omeprazole

ASJC Scopus subject areas

  • Physiology
  • Hepatology
  • Gastroenterology
  • Physiology (medical)


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