To observe the effects of total flavonoids from Ampelopsis grossedentata on glucose utilization in insulin resistance models of C2C12 myotube cells induced by palmitic acid,and to explore its mechanism from IRS-1/PI3K p85/AKT/GLUT4 signaling transduction pathways.Methods:Mouse C2C12 myoblasts were cultured in high glucose medium(DMEM) containing 2% horse serum,and then induced into mature myotube cells,which were cultured for 16 hours with 0.5mmol/L palmitic acid to establish the cellular insulin resistance models.The CCK-8 method was used to determine the effects of the total flavonoids from Ampelopsis grossedentata at different concentrations(5 μg/mL,10 μg/mL,20 μg/mL,30 μg/mL,50 μg/mL,80 μg/mL) on the activity of C2C12 cells,and determine the high,medium and low doses of total flavonoids from Ampelopsis grossedentata in subsequent experiments.The myotube cells induced by C2C12 cells were divided into normal group(NC),high glucose model group(DM) and total flavonoids from Ampelopsis grossedentata in high,medium,and low dose groups(AGH,AGM,AGL).The glucose consumption of each group cells was measured.Western Blotting was used to detect the effect of total flavonoids from Ampelopsis grossedentata on protein expressions of IRS-1/PI3K p85/AKT/GLUT4 signaling transduction.Results:When the total flavonoids from Ampelopsis grossedentata was 50 μg/mL,the cell survival rate was the highest.According to the detection of C2C12 cell viability,the high,medium,and low concentrations of total flavonoids from Ampelopsis grossedentata used in subsequent cell experiments were 80 μg/mL,50 μg/mL,and 30 μg/mL,respectively.Compared with the high glucose model group,the glucose consumption of total flavonoids from Ampelopsis grossedentata in the high,medium and low dose groups increased significantly(P<0.01).The high and medium dose groups of total flavonoids from Ampelopsis grossedentata significantly increased the protein expression of IRS-1/PI3K p85/AKT/GLUT4 signaling pathway(P<0.01).Conclusion:Total flavonoids of Ampelopsis grossedentata can improve the glucose consumption of C2C12 cells and thereby improve insulin resistance.Its mechanism of action may be achieved by regulating the IRS-1/PI3K p85/AKT/GLUT4 signaling pathway.