성능/효과

• Chronic treatment with fibroin fraction Fill showed two surprising results. First, fibroin treatment alone increased the relative amount of GLUT1 in both the PM and HDM fractions with no affect on the GLUT1 pool in the LDM fraction. Because the HDM represents the biosynthetic compartments (ER and Golgi), this suggests that the increase in GLUT1 arises from new synthesis.
• Because the HDM represents the biosynthetic compartments (ER and Golgi), this suggests that the increase in GLUT1 arises from new synthesis. The second surprise was that fibroin enhanced the redistribution of GLUT4 from the LDM fraction to the PM, independent of the presence of acute insulin addition although the response to fibroin was significantly less than the response to insulin. Little change in the expression of GLUT4 was noted, and were less reproducible that those of GLUT1.
• While the involvement of Akt in insulin-induced GLUT4 translocation is still controversial (28, 31-33), evidence has been reported which implicates Akt in the insulin-induced increase in GLUT1 expression (34). These investigators showed that dominant negative mutants of PI3-kinase and Akt blocked the insulin-induced increase in GLUT1 expression in 3T3-L1 adipocytes. Further, they showed that rapamycin, an inhibitor of mammalian target of rapamycin (mTOR), also blocked GLUT1 translation.