Department of Nutrition and Food Hygiene, School of Public Health, Peking University, Beijing 100191, PR China.
Phytomedicine. 2010 Jan;17(1):14-8. doi: 10.1016/j.phymed.2009.09.007. Epub 2009 Oct 12.
The tea polyphenol epigallocatechin-3-O-gallate (EGCG) displays some antidiabetic effects; however the mechanisms are incompletely understood. In the present study, the investigation of the effects of EGCG on insulin resistance was performed in rat L6 cells treated with dexamethasone. We found that dexamethasone increased Ser307 phosphorylation of insulin receptor substrate-1 (IRS-1) and reduced phosphorylation of AMPK and Akt. Furthermore, glucose uptake and glucose transporter (GLUT4) translocation were inhibited by dexamethasone. However, the treatment of EGCG improved insulin-stimulated glucose uptake by increasing GLUT4 translocation to plasma membrane. Furthermore, we also demonstrated these EGCG effects essentially depended on the AMPK and Akt activation. Together, our data suggested that EGCG inhibited dexamethasone-induced insulin resistance through AMPK and PI3K/Akt pathway.
表没食子儿茶素没食子酸酯（EGCG）显示出一些抗糖尿病作用；然而，其机制尚不完全清楚。在本研究中，我们研究了 EGCG 对用地塞米松处理的大鼠 L6 细胞胰岛素抵抗的影响。结果发现，地塞米松增加了胰岛素受体底物-1（IRS-1）的 Ser307 磷酸化，同时降低了 AMPK 和 Akt 的磷酸化。此外，地塞米松抑制了葡萄糖摄取和葡萄糖转运蛋白（GLUT4）易位。然而，EGCG 的处理通过增加 GLUT4 向质膜的易位来改善胰岛素刺激的葡萄糖摄取。此外，我们还证明了这些 EGCG 作用主要依赖于 AMPK 和 Akt 的激活。总之，我们的数据表明，EGCG 通过 AMPK 和 PI3K/Akt 通路抑制了地塞米松诱导的胰岛素抵抗。
