Abstract
The glucose absorption was measured from the small intestine of streptozotocin-induced (STZ) diabetic and Goto-Kakizaki (GK) rats, the Type 2 spontaneously diabetic model.
Control, STZ and GK rats were fasted and sacrificed, and then the small intestine was isolated and perfused in vitro. A Krebs-Ringer buffer containing either 60 or 300mg/dl of glucose was perfused from the superior mesenteric artery (SMA). After pre-perfusing for 20min, a 3% glucose solution was infused into the lumen from the duodenum for 30min. The total glucose absorption was calculated from the difference between the initial glucose concentration and that of the perfusate flowing out of the portal vein. The increase in the amount of glucose from the preperfusion was also calculated.
Decreased glucose absorption was observed in the control rats after the glucose infusion into the lumen, when the perfusate glucose concentration rose to a high level. Increased glucose absorption was observed in the STZ rats with a 300mg/dl perfusate glucose concentration when compared to that with a 60mg/dl concentration, and no decrease was apparent. The glucose absorption by the GK rats did not change at all.
These results suggest that the insulin-deficient STZ rats and spontaneously diabetic GK rats each showed an abnormal glucose absorption mechanism. Hyperglycemia may be attributable to a malfunction of the absorption mechanism.
