Antidiabetic mechanism of Bakumondo-inshi.
To determine the antidiabetic mechanism of Bakumondo-inshi (BI), we examined its effects on glucose absorption, alpha-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 alpha-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 alpha-glucosidase activity. Because of its therapeutic mechanism, BI could be a new category of therapeutic agent for non-insulin dependent diabetic mellitus.
D000818:Animals; D015153:Blotting, Western; D004365:Drugs, Chinese Herbal / Q000494:pharmacology*; D005947:Glucose / Q000378:metabolism; D051296:Glucose Transporter Type 5; D007004:Hypoglycemic Agents / Q000494:pharmacology*; D007408:Intestinal Absorption / Q000187:drug effects; D007421:Intestine, Small / Q000378:metabolism; D008297:Male; D051379:Mice; D009004:Monosaccharide Transport Proteins / Q000378:metabolism; D000520:alpha-Glucosidases / Q000378:metabolism