Activation of AMPK and PPARγby emodin influences glucose uptake in 3 T3-L1 adipocytes / 中国药理学通报

ABSTRACT

Aim To investigate glucose uptake effects and mechanism of emodin in 3T3-L1 adipocytes. Methods LPS-induced differentiated 3 T3-L1 adipo-cytes were divided into control group and emodin ( 1 , 10, 50 μmol · L-1 ) groups. Then, 6-NBDG uptake and the expression of cell surface GLUT4 , PPARγ, AMPKα1/2 , p-AMPKα1/2 , IRS-1 , p-IRS-1 , Adi-ponectin, chREBP-α and chREBP-β were detected. The ability of 6-NBDG uptake in LPS-induced 3 T3-L1 adipocytes was also evaluated following interference with AMPK inhibitor and PPARγinhibitor, respective-ly. Meanwhile, STZ-induced diabetic rats were ran-domly divided into control group and emodin treatment group. The mRNA expression of Adiponectin and pro-tein expression of cell surface GLUT4 , AMPKα1/2 , p-AMPKα1/2 were measured. Results Compared with the control group, emodin improved the mRNA expres-sion of cell surface GLUT4, Adiponectin, chREBP-αand chREBP-β, and protein expression of cell surface GLUT4 , PPARγ, IRS-1 , p-IRS-1 , AMPKα1/2 and p-AMPKα1/2 in 3T3-L1 adipocytes(P<0. 05). Emodin enhanced 6-NBDG uptake and the uptake of emodin group was both decreased following interference with AMPK inhibitor and PPARγ inhibitor, respectively ( P<0. 05 ) . Emodin also increased the mRNA expression of Adiponectin and protein expression of cell surface GLUT4 , AMPKα1/2 and p-AMPKα1/2 in adipose tis-sue of T2 DM rats ( P <0. 05 ) . Conclusion Emodin can enhance glucose uptake in 3 T3-L1 adipocytes and the mechanism is probably associated with activating Adiponectin and IRS-1 , thereby activating AMPK and PPARγ.