β-ecdysterone from Cyanotis arachnoidea exerts hypoglycemic effects through activating IRS-1/Akt/GLUT4 and IRS-1/Akt/GLUT2 signal pathways in KK-Ay mice

Abstract

Our present study investigated the anti-diabetic activity and potential mechanism of β-ecdysterone (β-EC) derived from Cyanotis arachnoidea. In vitro, β-EC exhibited a promising effect on increasing GLUT4 translocation by 1.6 folds and glucose uptake by 1.75 folds in L6 cells. In vivo, KK-Ay mice’s body weight, blood glucose levels and other related blood–lipid indexes can be significantly reduced with β-EC treatment. For the mechanism study, we have found that β-EC exhibited a significant protective effect on insulin resistance (IR) in L6 and HepG2 cells through increasing expressions of IRβ, p-Akt, p-IRS-1 and increasing the expressions of GLUT4 and GLUT2. The phosphorylation of Akt, IRS-1 and the expression of IRβ, GLUT4 and GLUT2 in the liver and skeletal muscle in KK-Ay mice were also significantly ameliorated after 4-weeks treatment with β-EC. According to our present findings, we could conclude that β-EC possessed the potential anti-diabetic effects through activating IRS-1/AKT/GLUT4 and IRS-1/AKT/GLUT2 pathways.

Keywords

• Hypoglycemic
• β-ecdysterone
• GLUT4
• Akt
• IRS-1
• IRβ