Research Paper Volume 11, Issue 18 pp 7510—7524
MiR-27a promotes insulin resistance and mediates glucose metabolism by targeting PPAR-γ-mediated PI3K/AKT signaling
Figure 6. Effects of miR-27a on the PI3K/Akt signaling pathways in IR 3T3-L1 cells. (A) Glucose level was examined in IR 3T3-L1 cells that underwent different treatments to assess the effects of PI3K inhibitor wortmannin (2.5 μM) on insulin sensitivity. (B) WB was performed to examine the PPAR-γ, Akt, GLUT expression, and Akt phosphorylation in cells transfected with agomiR-27a and/or treated with wortmannin. (C) qPCR determined that the PPAR-γ expression was not inhibited by wortmannin (2.5 μM) for 24h. (D) Image pixel analysis showed phosphorylated level Akt protein after wortmannin treatment. (E) qPCR was performed to confirm that wortmannin treatment downregulated the glucose level that was induced by agomiR-27a transfection. Number = 3. *P < 0.05 vs. indicated groups.