Intragastric administration of a liposomal surfactant suspension markedly reduced acid-induced gastric ulcerogenesis and bleeding in rats. The concentration of surface-active molecules intrinsically present in the gastric mucosa was increased two to six times by administration of 16,16-dimethyl prostaglandin E2. Thus, local accumulation of surface-active phospholipids may be an integral component of the cytoprotective mechanism activated by prostaglandin treatment.

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The dietary chemical constituents responsible for initiating the gastrin secretory response to a meal have yet to be identified. The evidence supporting the importance of dietary amino acids in the initiation of the postprandial release of gastrin is both conflicting and unconvincing. In this study we investigated the role of the amino acid breakdown products ammonia and the amines in the regulation of gastrin release both in vivo and in vitro. Lyophilization of standard rat food under alkaline conditions results in the volatilization of both ammonia and the amines, which can be subsequently condensed in a cold trap. The normal postprandial release of gastrin is significantly reduced by approximately 50% when rats are fed this freeze-dried diet. Addition of the amine-containing condensate back to the freeze-dried diet completely restores this response to normal. Analysis of the completely restores this response to normal. Analysis of the condensate by thin-layer chromatography revealed that it contained ammonia, methylamine, ethylamine, dimethylamine, and a fourth unidentified aliphatic amine. All of the above compounds significantly stimulated the release of gastrin from isolated G cells. Similarly, addition of ammonia and a synthetic amine mixture to the freeze-dried diet completely restored the postprandial release of gastrin to normal levels. In conclusion, our results suggest that dietary amines and ammonia may play a key role in initiating the gastrin secretory response to a meal.

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