Antidiabetic Mechanism of Bakumondo-inshi

抄録

To determine the antidiabetic mechanism of Bakumondo-inshi (BI), we examined its effects on glucose absorption, α-glucosidase activity, sodium-dependent glucose transporter and facilitative glucose transporter isoform 5 (GLUT5) in small intestine. The oral administration of BI into KK-Ay mice caused a significant decrease in the glucose absorption in small intestine. The small intestine content of active glucose transporter isoform (SGLUT) protein content from KK-Ay mouse significantly decreased in the BI-treated KK-Ay mice compared to that in the controls. However, the small intestine content of facilitative glucose transporter isoform, GLUT5 protein content did not change. The α-glucosidase activity in small intestine significantly decreased in the BI-treated KK-Ay mice. These results suggest that the antidiabetic effect of BI is derived, at least in part, from a decrease of glucose absorption in small intestine, due to the reduction of SGLUT protein content in total membrane of the small intestine and the reduction of α-glucosidase activity. Because of its therapeutic mechanism BI could be a new category of therapeutic agent for non-insulin dependent diabetic mellitus.