Concomitant onset of hypergastrinemia, intragastric alkalinity and gastric hyperplasia, and numbers of antral G cells in Taenia taeniaeformis-infected rats

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Infection of hepatic larvae of Taenia taeniaeformis is associated with gastropathy in rats. The sequence of occurrence of the prominent changes, i.e. gastric hyperplasia, intragastric alkalinity and hypergastrinemia, could provide an insight on the pathogenetic mechanism(s) involved in the induction of gastric changes. Density of gastrin producing antral G cells was also examined to determine the cause of hypergastrinemia. Five-week-old, male Wistar rats were orally infected with approximately 4000 Taenia taeniaeformis eggs and examined for changes of stomach morphology, intragastric pH, and serum gastrin every 2 weeks post-infection. Numbers of antral G cells were determined by quantitative immunohistochemistry. Gastric hyperplasia, hypergastrinemia, and rise of intragastric pH occurred concomitantly 56 days post-infection. Mean number of G cells per 100 μm 2 antral mucosa in infected rats was comparable to uninfected controls, although there was an apparent increase in width of antral mucosal sections in hyperplastic stomachs. The concomitant onset of gastric hyperplasia, intragastric alkalinity and hypergastrinemia, most likely indicate that chemical mediators are involved which primarily mediate rapid hyperplasia of mucus-secreting cells. Hypergastrinemia associated with this condition could be due to antral G-cell hyperfunction. However, an increase in total antral G-cell population should be considered because of gross enlargement of hyperplastic stomachs.