RATS WITH GASTRITIS HAVE INCREASED SENSITIVITY TO THE GASTRIN STIMULATORY EFFECTS OF LUMINAL AMMONIA

Background & Aims: Persons infected with Helicobacter pylori show an e nhanced meal-stimulated gastrin release compared with uninfected contr ols. The aim of this study was to determine in animal models whether t his gastrin release could be related to chronic gastric inflammation, elevated luminal ammonia level, or a combination of these factors. Met hods: Two rat models of mild gastric inflammation were studied. Rats g iven a long-term diet of 20 g/dL ammonium acetate (AmAc) in vat chow o r 0.1% iodoacetamide in drinking water for 2-3 weeks underwent a short -term challenge with a normal or AmAc-supplemented meal. Serum gastrin and antral gastrin messenger RNA levels were measured. Results: Compa red with normal postprandial gastrin release, animals given the long-t erm AmAc feeding showed a normal response to rat chow but a greatly ex aggerated response to rat chow plus 20 g/dL AmAc. Long-term feeding wi th iodoacetamide also resulted in enhanced gastrin release and antral gastrin messenger RNA in response to a meal supplemented with AmAc, bu t not to a normal meal or one supplemented with sodium acetate. Conclu sions: Inflamed gastric mucosa is move sensitive to the effects of lum inal ammonia and responds with an increase in both synthesis and relea se of gastrin. These animal models may provide insight into the pathog enesis of hypergastrinemia associated with ii. pylori infection.