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It has been shown that those factors which affect gastric acid secretion through the ventromedial and lateral nuclei of hypothalamus, can significantly alter centrally-mediated secretion. There is much evidence that glucose is among these factors that through a central mechanism can decrease induced acid secretion. It appears that this effect is mediated through glucose-sensitive neurons within lateral (LH) and ventromedial (VMH) nuclei of hypothalamus. Therefore, this study was carried out to evaluate the effect of D-glucose injection into LH and VMH on pentagastrin-induced hyperacidity in anesthetized rats. After induction of anesthesia, guide cannula was stereotaxically inserted 1 mm above VMH and/or LH of both sides. Then, after 3-7 days the stomach was washed out, and from 15 min on, sampling (every 5 min) from gastric secretion was done until the end of experiment. Venous infusion of pentagastrin (2 µg/100 g/h) increased acid secretion and it reached to its maximum level after 30 min. The results showed that D-glucose injection (10, 20, 30, and 90 mM) at a rate of 1 µl/rat significantly and in a dose-dependent manner reduce acid secretion, while L-glucose injection (30 mM) or saline solution (154, 169, and 200 mM) did not significantly affect acid secretion. It can be concluded that the VMH and LH contain glucose-sensitive neurons that can influence gastric acid secretion, and D-glucose can be effective on these neurons, which through this way can reduce peripherally-induced hyperacidity. In addition, this effect is stronger at LH than VMH, and the other analogue of glucose (L-glucose) can not affect this phenomenon.

Keywords: Lateral and Ventromedial nuclei of hypothalamus; Hyperacidity; Gastrin; D-glucose