Background & aims: Persons infected with Helicobacter pylori show an enhanced meal-stimulated gastrin release compared with uninfected controls. The aim of this study was to determine in animal models whether this gastrin release could be related to chronic gastric inflammation, elevated luminal ammonia level, or a combination of these factors.
Methods: Two rat models of mild gastric inflammation were studied. Rats given a long-term diet of 20 g/dL ammonium acetate (AmAc) in rat chow or 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: Compared with normal postprandial gastrin release, animals given the long-term AmAc feeding showed a normal response to rat chow but a greatly exaggerated response to rat chow plus 20 g/dL AmAc. Long-term feeding with iodoacetamide also resulted in enhanced gastrin release and antral gastrin messenger RNA in response to a meal supplemented with AmAc, but not to a normal meal or one supplemented with sodium acetate.
Conclusions: Inflamed gastric mucosa is more sensitive to the effects of luminal ammonia and responds with an increase in both synthesis and release of gastrin. These animal models may provide insight into the pathogenesis of hypergastrinemia associated the H. pylori infection.