Epigallocatechin gallate promotes GLUT4 translocation in skeletal muscle
Epigallocatechin gallate promotes GLUT4 translocation in skeletal muscle
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DOI：
10.1016/j.bbrc.2008.09.128
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发表时间：
2008-12-05
影响因子：
3.1
通讯作者：
Ashida, Hitoshi
中科院分区：
文献类型：
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作者：
Ueda, Manabu;Nishiumi, Shin;Ashida, Hitoshi
本研究探讨了表没食子儿茶素没食子酸酯（EGCg）对骨骼肌葡萄糖摄取活性和胰岛素敏感葡萄糖转运蛋白（GLUT）4转位的影响。单次口服给予75 mg/kg体重的EGCg可促进大鼠骨骼肌中GLUT 4易位。EGCg在1 nM时显著增加L 6肌管中伴随GLUT 4易位的葡萄糖摄取。在小鼠和大鼠离体骨骼肌和胰岛素抵抗的L 6肌管中也观察到GLUT 4的易位。磷脂酰肌醇3 '-激酶抑制剂渥曼青霉素可抑制EGCg和胰岛素增加的葡萄糖摄取，而酪氨酸激酶抑制剂染料木黄酮则不能抑制EGCg增加的葡萄糖摄取。因此，ECCg可能通过促进骨骼肌GLUT 4转位来改善高血糖，其机制与胰岛素部分不同。(C)2008年爱思唯尔公司All rights reserved.
In this study, We investigated whether epigallocatechin gallate (EGCg) affects glucose uptake activity and the translocation Of insulin-sensitive glucose transporter (GLUT) 4 in skeletal muscle. A single oral administration of EGCg at 75 mg/kg body weight promoted GLUT4 translocation in skeletal muscle of rats. EGCg significantly increased glucose uptake accompanying GLUT4 translocation in L6 myotubes at 1 nM. The translocation of GLUT4 was also observed both in skeletal muscle of mice and rats ex vivo and in insulin-resistant L6 myotubes. Wortmannin, an inhibitor of phosphatidylinositol 3'-kinase, inhibited both EGCg- and insulin-increased glucose uptakes, while genistein, an inhibitor of tyrosine kinase, failed to inhibit the EGC-increasecl uptake. Therefore, ECCg may improve hyperglycemia by promoting GLUT4 translocation in skeletal muscle with partially different mechanism from insulin. (C) 2008 Elsevier Inc. All rights reserved.