Btd-1

Btd-1

Description

BTD-1 is soybean-fermented extract which can inhibit the elevation of postprandial blood glucose level. For producing BTD-1, defatted soybean meal as medium is fermented by Bacillus subtilis MORI, a patented strain(KCCM-10450P), isolated from a Korean traditional food, Chungkookjang. B. subtilis MORI can produce 1-deoxynojirimycin(DNJ) which has high inhibitory activity against α-glucosidase. Therefore, BTD-1 can control blood glucose level. Characteristics of BTD-1 α-glucosidase inhibitors inhibit α-glucosidase related to carbohydrate digestion in the small intestine and then reduce increase of postprandial blood glucose level (Fig. 2). Most carbohydrates in food consist of starch and sucrose. These carbohydrates are digested by pancreatic α-amylase and α-glucosidase in the villi of the small intestine and consequently the level of blood glucose level increases at rapid rate. Therefore, α-glucosidase inhibitors can inhibit the sharp peak of postprandial blood glucose level.

According to the experiment of type 2 DM, the administration of BTD-1 can significantly normalize fasting blood glucose, postprandial 2h blood glucose level and HbA1c (Fig. 4). As a result, the pancreatic islet architecture was preserved and plasma.

Effect of 1-BTD on the prevention of diabetes complications

In order to scavenge oxygen free radicals produced from DM induction, BTD-1 can elevate enzymatic oxidants such superoxide dismutase, glutathione peroxidase and catalase and prevent from the cell damages. In addition, the administration of BTD-1 prevents from free radical- mediated oxidative stress in vascular endothelium cells and maintains vascular compliance. 

Additionally BTD-1 can induce transportation of glucose from blood into cells and reduce the blood glucose level.
Glucose transporter type 4 (GLUT4) is a protein which is the insulin-regulated glucose transporter. In order to transport glucoses into cells, GLUT4 moves to cell membrane. In normal condition, most GLUT4 present in cytoplasm, but the GLUT4 shifts to cell membrane when insulin is treated to cells. Treatment of BTD-1 induced GLUT4s to move in cell membrane. Therefore, BTD-1 may play a role like insulin to GLUT4.


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