Abstract: 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.

Key words: Palmitate, Skeletal muscle, L6GLUT4myc, Translocation, Insulin resistance