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ObjectiveTo investigate the effects of zinc on glucose consumption in normal and insulin-resistant L6 myotubes and elucidate its association with AKT/GSK3β phosphorylation, two key components in the insulin-signaling pathway.Methods The insulin-resistant cell model was prepared by treating L6 myotubes with 0.4mmol/L palmitic acid for 24h and then exposed to different concentrations of zinc (0, 10, 20, 50, 100μmol/L) in the presence or absence of insulin (100 nmol/L) for 3h. Glucose consumption was determined by glucose oxidase method. AKT /GSK3β phosphorylation was detected by West blotting method.ResultsIn normal L6 myotubes, zinc (10-50μmol/L) alone could significantly increase glucose consumption. In the presence or absence of insulin, zinc significantly enhanced AKT/GSK3β phosphorylation. In insulin-resistant L6 myotubes, zinc (10-50μmol/L) could increase glucose consumption and GSK3β phosphorylation, which was accompanied by enhanced AKT phosphorylation in the presence of insulin.ConclusionCollectively, these results showed that zinc at the concentrations of 10-50μmol/L could increase glucose consumption in L6 myotubes. The mechanism was related to the activation of the insulin signaling pathway by zinc through AKT/GSK3β phosphorylation.