The effect of intragastric D-glucose on hyperacidity induced by histamine and carbachol in male rat

It has been shown that enhanced acid secretion can be suppressed in the rat by systemic administration of glucose. We have recently reported that enhancement of acid secretion as a result of pentagastrin was diminished by intragastric administration of D-glucose. Present study was designed to investigate whether intragastric D-glucose influences gastric acid secretion associated with carbachol and histamine in rat, and then we compared these results with our previous results obtained by pentagastrin-induced hyperacidity. Intravenous infusion of carbachol (1 mg/100 g/h) and histamine (0.5 mg/100 g/h) caused an immediate increase in acid secretion with a peak starting after 40 and 60 min and then reached to a steady state respectively. 1ntragastric administration of D-glucose significantly reduced the hyperacidity induced by histamine and carbachol (p<0.01). The effect of intragastric D-glucose on hyperacidity induced by pentagastrin or histamine when compared with carbachol-induced hyperacidity was significantly greater than carbachol group. In conclusion, it is suggested that the inhibitory effect of intragastric D-g1ucose observed in hyperacidity may be the result of glucose-induced modification of intragastric pathways in parietal cells that control gastric acid secretion.