锌对L6细胞葡萄糖消耗量和蛋白激酶B/糖原合酶激酶3β表达的影响（英文）

Effects of Zinc on Glucose Consumption and AKT/GSK3β Phosphorylation in L6 Myotubes

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 in normal and insulin-resistant L6 myotubes and elucidate its association with AKT/GSK313 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, 100 μmol/L） in the presence or absence of insulin （100 nmol/L） for 3h. Glucose consumption was determined by glucose oxidase method. AKT /GSK31β phosphorylation was detected by Western blotting method. Results In normal L6 myotubes, zinc （10-50μmol/L） alone could significantly increase glucose consumption. In the presence or absence of insulin, zinc significantly enhanced AKT/GSK313 phosphorylation. In insulin-resistant L6 myotubes, zinc （10-50μmol/L） could increase glucose consumption and GSK313 phosphorylation, which was accompanied by enhanced AKT phosphorylation in the presence of insulin. Conclusion Collectively, these results showed that zinc at the concentrations of 10-50 μmol/L could increase glucose consumption in L6 myotubes. The mechanism was related to the activation of the insulin signaling pathway by zinc through AKT/GSK313 phosphorylation.