Fig. 5.

Targeting of hOGG1 to mitochondria in L6 myotubes protected against palmitate-induced decrease in insulin-stimulated 2DG uptake. A, MTS-hOGG1- and GFP-transduced L6 myotubes were treated with 2% BSA (C, 2% BSA) or 2% BSA plus 1 mm palmitate (P) for 16 h. After that, cells were incubated in the absence or presence of insulin for 20 min and then for 5 min with 2DG, and uptake was measured as described in Materials and Methods. Values were normalized to the GFP control basal data and are the means ± se (n ≥ 3). *, P < 0.05 vs. respective basal; #, P < 0.05 vs. all other groups treated with insulin. B, graph, Effect of a JNK inhibitor on palmitate-induced inhibition of insulin-stimulated 2DG uptake. L6 myotubes were incubated in the medium containing only 2% BSA (C, Control) (2% BSA) or 2% BSA plus 1 mm palmitate (P) in the presence or absence of the JNK inhibitor, SP-600125 for 16 h before stimulation with insulin and measurement of 2DG uptake. Values were normalized to the control basal data and are the means ± se (n ≥ 3). Δ, Fold induction on insulin. *, P < 0.05 vs. both control and palmitate plus SP-600125. B, panel above graph, Effect of JNK inhibitor on palmitate-induced mtDNA damage. L6 myotubes were incubated with 2% BSA (C) or 2% BSA plus 1 mm palmitate (P) in the presence or absence of the JNK inhibitor, SP-600125 for 6 h. mtDNA damage was evaluated as described in Materials and Methods.