Epigallocatechin-3-O-gallate (EGCG) protects the insulin sensitivity in rat L6 muscle cells exposed to dexamethasone condition

Abstract 

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.

Keywords: Epigallocatechin-3-O-gallate, Dexamethasone, Insulin resistance, Rat L6 muscle cells

Abbreviations: Akt, Protein kinase B, AMPK, AMP-activated protein kinase, EGCG, Epigallocatechin-3-O-gallate, FBS, Fetal bovine serum, GLUT4, Glucose transporter-4, IRS-1, Insulin receptor substrate-1, NGS, Normal goat serum, PI-3K, Phosphatidylinositol 3 kinase