JNK在棕榈酸造成骨骼肌细胞胰岛素抵抗中的作用

目的:探讨棕榈酸造成L6GLUT4myc骨骼肌细胞胰岛素抵抗的机制中，c-Jun N-末端激酶(JNK)的作用。方法:第一部分将细胞分两组，分别用0.3 mmol／L的棕榈酸盐或用溶剂牛血清白蛋白（BSA）孵育16 h；第二部分在如上处理的后30 min加入JNK的抑制剂，用或不用胰岛素刺激后，检测细胞膜上GLUT4myc的含量以及蛋白激酶B(Akt)、JNK和胰岛素受体底物1（IRS1）的磷酸化。结果：与溶剂组相比，棕榈酸组中胰岛素刺激的GLUT4myc转位和Akt的磷酸化降低(P<0.05)；JNK和IRS1Ser307的磷酸化水平则没有变化。结论：棕榈酸导致L6骨骼肌细胞胰岛素抵抗的机制可能不涉及JNK或JNK的作用很小。

The Role of JNK in the Mechanism of Palmitate-induced Insulin Resistance in Skeletal Muscle Cells

Objective: To study the role of c-Jun N-terminal kinase (JNK) in the mechanism of palmitate-induced insulin resistance in L6GLUT4myc skeletal muscle cells. Methods: In the first part of this study, L6GLUT4myc muscle cells were divided into two groups and treated with 0.3 mmol / L palmitate or solvent BSA for 16 h, respectively. In the second part of this study, JNK inhibitor was added to the medium during the last 30 min incubation with palmitate or BSA. The amount of GLUT4myc on the cell surface and the phosphorylation of protein kinase B (Akt), JNK and insulin receptor substrate1 (IRS1) were measured in the absence or presence of insulin respectively. Results: Compared to the solvent group, insulin-stimulated GLUT4myc translocation and phosphorylation of Akt decreased in palmitate group (P <0.05); phosphorylation of JNK and IRS1Ser307 did not change. Conclusion: Palmitate causes insulin resistance in L6 muscle cells, and its mechanism may not involve JNK, or JNK plays a minor role.