Tea catechins modulate the glucose transport system in 3T3-L1 adipocytes.
Tea catechins modulate the glucose transport system in 3T3-L1 adipocytes.
复制标题
DOI：
10.1039/c0fo00105h
复制
发表时间：
2010-11
期刊：
影响因子：
6.1
通讯作者：
Manabu Ueda;T. Furuyashiki;Kayo Yamada;Yukiko Aoki;I. Sakane;I. Fukuda;Ken-ichi Yoshida;H. Ashida-H.-A
中科院分区：
文献类型：
--
作者：
Manabu Ueda;T. Furuyashiki;Kayo Yamada;Yukiko Aoki;I. Sakane;I. Fukuda;Ken-ichi Yoshida;H. Ashida-H.-A
在本研究中，我们研究了茶儿茶素对3T3-L1脂肪细胞葡萄糖转运蛋白(GLUT)4转位的影响。我们发现，绿茶提取物中含有丰富儿茶素的乙酸乙酯部分，在3T3-L1细胞中最能降低胰岛素诱导的葡萄糖摄取活性。当50μM儿茶素在无胰岛素或有胰岛素的情况下处理细胞30min时，无胰岛素时，非没食子酸型儿茶素可增加葡萄糖摄取活性，而没食子酸型儿茶素则降低胰岛素诱导的葡萄糖摄取活性。非儿茶酸型儿茶素(-)-表没食子儿茶素(EC)和(-)-表儿茶素(EGC)以剂量和时间依赖方式增加葡萄糖摄取活性，而(-)-儿茶素3-没食子酸酯(CG)和(-)-表没食子儿茶素3-没食子酸酯(EGCG)以剂量和时间依赖方式降低胰岛素诱导的葡萄糖摄取活性。当50μM儿茶素处理细胞30min时，EC和EGCG促进GLUT4易位，而CG和EGCG则抑制胰岛素诱导的细胞内GLUT4易位。EC和EGC可增加PKCλ/ζ的磷酸化，而不增加胰岛素受体(IR)和AKT的磷酸化。磷脂酰肌醇3‘-激酶(PI3K)抑制剂Wortmannin和LY294002可降低EC和EGC诱导的细胞葡萄糖摄取活性。在胰岛素存在的情况下，CG和EGCG降低了PKCλ/ζ的磷酸化，但不影响胰岛素诱导的IR和Akt的磷酸化。因此，EC和EGC通过激活PI3K促进GLUT4的转位，CG和EGCG通过胰岛素信号转导途径抑制胰岛素诱导的GLUT4转位。
In this study, we investigated the effects of tea catechins on the translocation of glucose transporter (GLUT) 4 in 3T3-L1 adipocytes. We found that the ethyl acetate fraction of green tea extract, containing abundant catechins, most decreased insulin-induced glucose uptake activity in 3T3-L1 cells. When the cells were treated with 50 μM catechins in the absence or presence of insulin for 30 min, nongallate-type catechins increased glucose uptake activity without insulin, whereas gallate-type catechins decreased insulin-induced glucose uptake activity. (-)-Epicatechin (EC) and (-)-epigallocatechin (EGC), nongallate-type catechins, increased glucose uptake activity in the dose- and time-dependent manner, whereas (-)-catechin 3-gallate (Cg) and (-)-epigallocatechin 3-gallate (EGCg), gallate-type catechins, decreased insulin-induced glucose uptake activity in the dose- and time-dependent manner. When the cells were treated with 50 μM catechins for 30 min, EC and EGC promoted GLUT4 translocation, whereas Cg and EGCg decreased the insulin-induced translocation in the cells. EC and EGC increased phosphorylation of PKCλ/ζ without phosphorylation of insulin receptor (IR) and Akt. Wortmannin and LY294002, inhibitors for phosphatidylinositol 3'-kinase (PI3K), decreased EC- and EGC-induced glucose uptake activity in the cells. Cg and EGCg decreased phosphorylation of PKCλ/ζ in the presence of insulin without affecting insulin-induced phosphorylation of IR, and Akt. Therefore, EC and EGC promote the translocation of GLUT4 through activation of PI3K, and Cg and EGCg inhibit insulin-induced translocation of GLUT4 by the insulin signaling pathway in 3T3-L1 cells.