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茶儿茶素调节 3T3-L1 脂肪细胞的葡萄糖转运系统。

Tea catechins modulate the glucose transport system in 3T3-L1 adipocytes.

机构信息

Department of Agrobioscience, Graduate School of Agricultural Science, Kobe University, Kobe 657-8501, Japan.

出版信息

Food Funct. 2010 Nov;1(2):167-73. doi: 10.1039/c0fo00105h. Epub 2010 Oct 21.

Abstract

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.

摘要

在这项研究中,我们研究了茶儿茶素对 3T3-L1 脂肪细胞中葡萄糖转运蛋白(GLUT)4转位的影响。我们发现,绿茶提取物的乙酸乙酯部分含有丰富的儿茶素,最能降低 3T3-L1 细胞中胰岛素诱导的葡萄糖摄取活性。当细胞用 50 μM 儿茶素处理,无论是否存在胰岛素 30 分钟时,非没食子酸儿茶素在没有胰岛素的情况下增加葡萄糖摄取活性,而没食子酸儿茶素则降低胰岛素诱导的葡萄糖摄取活性。(-)-表儿茶素(EC)和(-)-表没食子儿茶素(EGC),非没食子酸儿茶素,以剂量和时间依赖的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),没食子酸儿茶素,以剂量和时间依赖的方式降低胰岛素诱导的葡萄糖摄取活性。当细胞用 50 μM 儿茶素处理 30 分钟时,EC 和 EGC 促进 GLUT4 转位,而 Cg 和 EGCg 则减少细胞中胰岛素诱导的转位。EC 和 EGC 增加 PKCλ/ζ的磷酸化,而不磷酸化胰岛素受体(IR)和 Akt。wortmannin 和 LY294002,磷脂酰肌醇 3'-激酶(PI3K)的抑制剂,降低了细胞中 EC 和 EGC 诱导的葡萄糖摄取活性。Cg 和 EGCg 在胰岛素存在的情况下降低 PKCλ/ζ的磷酸化,而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,而 Cg 和 EGCg 通过胰岛素信号通路抑制胰岛素诱导的 GLUT4 转位。

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