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目的以L6细胞为研究对象,观察锌对正常L6细胞及棕榈酸诱导的胰岛素抵抗L6细胞葡萄糖消耗量及胰岛素信号通路关键分子蛋白激酶B(protein kinase B,PKB/AKT)/糖原合成酶激酶3β(glycogen synthase kinase,GSK3β)表达的影响。方法培养L6成肌细胞,分化后用0.4 mmol/L棕榈酸作用24h造胰岛素抵抗细胞模型,用100 nmol/L胰岛素和不同浓度的锌(0,10,20,50,100μmol/L)作用3h,葡萄糖氧化酶法测定基础状态和胰岛素刺激状态下细胞对葡萄糖的摄取量;用100 nmol/L胰岛素和不同浓度的锌(0,10,20,50μmol/L)作用15 min,Western blot法检测磷酸化AKT及磷酸化GSK3β表达水平。结果 10~50μmo/L的锌能明显提高正常L6细胞葡萄糖的消耗量和AKT/GSK3β的磷酸化表达,锌与胰岛素共刺激能显著激活AKT/GSK3β;而对于胰岛素抵抗L6细胞,10~50μmo/L锌单独作用可明显提高其葡萄糖消耗量和GSK3β的磷酸化,10~50μmo/L锌与胰岛素共刺激能激活AKT的磷酸化表达。结论10~50μmol/L的锌可提高L6细胞的葡萄糖消耗量,这种作用可能与其增强AKT和GSK3β磷酸化水平有关。
Objective To investigate the effects of zinc on glucose consumption and the protein kinase B (PKB / AKT) / glycogen synthase kinase in normal L6 cells and palmitate-induced insulin resistance L6 cells 3β (glycogen synthase kinase, GSK3β) expression. Methods L6 myoblasts were cultured and treated with 0.4 mmol / L palmitic acid for 24 h to induce insulin resistant cell line. The cells were treated with 100 nmol / L insulin and different concentrations of zinc (0, 10, 20, 50 and 100 μmol / L) for 3 h, Glucose oxidase method was used to measure the uptake of glucose by basal cells and insulin stimulated cells.Using 100 nmol / L insulin and different concentrations of zinc (0, 10, 20 and 50 μmol / L) for 15 min, AKT and phosphorylated GSK3β expression levels. Results Zinc (10-50 μmol / L) significantly increased glucose consumption and phosphorylation of AKT / GSK3β in normal L6 cells. Co-stimulation with zinc and insulin significantly activated AKT / GSK3β. For insulin-resistant L6 cells, L zinc alone can significantly improve its glucose consumption and GSK3β phosphorylation, 10 ~ 50μmo / L zinc and insulin co-stimulation can activate AKT phosphorylation. Conclusion 10 ~ 50μmol / L zinc can increase the glucose consumption of L6 cells, which may be related to the enhancement of AKT and GSK3β phosphorylation.