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

被引:15
作者
Chen, Li [1 ]
Zheng, Sijian [1 ]
Huang, Mi [1 ]
Ma, Xinhua [1 ]
Yang, Jie [1 ]
Deng, Shihao [1 ]
Huang, Yun [1 ]
Wen, Yanzhang [1 ]
Yang, Xinzhou [1 ]
机构
[1] South Cent Univ Nationalities, Sch Pharmaceut Sci, 182 Min Zu Rd, Wuhan 430074, Hubei, Peoples R China
基金
中国国家自然科学基金;
关键词
Hypoglycemic; beta-ecdysterone; GLUT4; Akt; IRS-1; IR beta; INSULIN-RESISTANCE; GLUCOSE-TRANSPORTER; ANTIDIABETIC ACTIVITY; GLUT4; TRANSLOCATION; MUSCLE; HYPERGLYCEMIA; OBESITY; INFLAMMATION; APOPTOSIS; EXTRACT;
D O I
10.1016/j.jff.2017.09.061
中图分类号
TS2 [食品工业];
学科分类号
0832 ;
摘要
Our present study investigated the anti-diabetic activity and potential mechanism of O-ecdysterone (beta-EC) derived from Cyanotis arachnoidea. In vitro, beta-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 beta-EC treatment. For the mechanism study, we have found that beta-EC exhibited a significant protective effect on insulin resistance (IR) in L6 and HepG2 cells through increasing expressions of IR beta, p-Akt, p-IRS-1 and increasing the expressions of GLUT4 and GLUT2. The phosphorylation of Akt, IRS-1 and the expression of itzp, GLUT4 and GLUT2 in the liver and skeletal muscle in KK-Ay mice were also significantly ameliorated after 4-weeks treatment with beta-EC. According to our present findings, we could conclude that beta-EC possessed the potential anti-diabetic effects through activating IRS-1/AKT/GLUT4 and IRS-1/AICT/GLUT2 pathways. (C) 2017 Elsevier Ltd. All rights reserved.
引用
收藏
页码:123 / 132
页数:10
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