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Objective To evaluate the effects of transcription factor 7-like 2 (TCF7L2) silence on the expression of insulin degrading enzyme (IDE) in insulin resistance (IR) model HepG2 cells and its possible mechanism. Methods The HepG2 cells were divided into blank group, TCF7L2 interference group, empty vector group, IR group, IR+TCF7L2 interference group and IR+empty vector group. IR-HepG2 cell model was induced by in vitro cultivation of the cells in high concentration of insulin (5×10-6 mol/L) for 24 hours; GOD-POD and 2-NBDG method was used to verify successful reproduction of IR-cell model. TCF7L2 specific siRNA lentivirus vector (LV-TCF7L2-siRNA) was constructed with TCF7L2 mRNA coding sequence as the interference target, and it was used to transfect the cells in blank group and IR group. Empty vector virus was used to transfect the cells in empty vector group and IR+empty vector group. The expressions of TCF7L2 and IDE mRNA were detected by qRT-PCR, and the changes in the expression of TCF7L2, IDE, insulin stimulated protein kinase B(AKT) and phosphorylated protein kinase B(p-AKT) were detected by Western blotting. The uptake rate of 2-deoxy-D-glucose (2-NBDG) was analyzed by flow cytometry. Results Compared with that in control group, the glucose consumption and the uptake rate of 2-NBDG significantly decreased in IR group (P |
