JNK在棕榈酸致骨骼肌细胞胰岛素抵抗中的作用

摘要

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: L6GLUT4myc myohlasts were inrubated in 24 and 6 wells plates and divided into two groups, and treated with 0.3 mmol/ L palmitate or solvent BSA for 16 h, respectively. 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 was measured by enzyme linked immunosorbent assay (ELISA) and the phosphorylation of protein kinase B (Akt).JNK and insulin receptor substratel (IRSI) were measured by immunoblotting in the ahsence 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). There was no significant difference in the phosphorylation of JNK and IRS1 pS307.Conclusion : Palmitate causes insulin resistance in L6 muscle cells, and JNK may not be involved in its mechanism.%目的:探讨棕榈酸造成L6GLUT4myc骨骼肌细胞胰岛素抵抗过程中c-Jnn N-末端激酶(JNK)所起的作用.方法:将L6GLUT4myc成肌细胞培养于24孔和6孔培养板中,随机分为溶剂组和棕榈酸组,分别用0.3 mmol/L的棕榈酸盐和溶剂牛血清白蛋白(BSA)孵育16h,在棕榈酸组的后30min加入JNK的抑制剂,于胰岛素刺激前后用酶联免疫吸附测定(ELISA)细胞膜上GLUT4myc的含量,免疫印迹法测定蛋白激酶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,棕榈酸组中胰岛素增加的GLUT4myc水平的倍数和Akt的磷酸化降低(P＜0.05);JNK和IRSI的丝氨酸位点S307的磷酸化水平变化差异无统计学意义(P＞0.05).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.