Acute high blood glucose level attenuates the formation of gastric ulcers in male Wistar rats

Studies have shown that hyperglycemic state induced by intravenous glucagon or glucose infusion may lead to inhibition of gastric acid secretion through the inhibition of gastric vagal activity. Conversely, hypoglycemic state has been reported to cause an increase in gastric acid secretion by increasing vagal stimulation. The gastrointestinal side effects of non-steroidal anti-inflammatory drugs (NSAIDs), especially on the stomach, are one of the more serious complications in individuals taking these drugs. The aim of this study was therefore to study the effect of a high or low blood glucose level on gastric ulcers formation induced by NSAID, indomethacin. Thirty male Wistar rats weighing between 200 and 250g were randomly divided into three groups of 10 rats each, receiving intravenous infusion of normal saline (control; group 1), glucose (hyperglycemic; group 2) or insulin (hypoglycemic; group 3) followed by oral administration of indomethacin (25mg/kg). The animals were sacrificed 4 hours after indomethacin administration and the stomach was removed to estimate the ulcer score (US). The ulcer score was significantly reduced in the hyperglycemic group compared to the control group, while no significant change was observed in the hypoglycemic group. In conclusion, these results indicate that high blood glucose levels attenuate the formation of NSAID-induced gastric ulcers while insulin-induced hypoglycemic state may not affect the formation of NSAID-induced gastric ulcers.