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. 2018 May 23;59(7):1148–1163. doi: 10.1194/jlr.M080788

Fig. 3.

Fig. 3.

Inhibition of the de novo pathway with myriocin does not reverse palmitate-induced insulin resistance and inflammation. Myotubes were pretreated with myriocin (25 μM) or the methanol (MeOH) vehicle for 30 min and then incubated with 0.5 mM PA in the presence of myriocin for 18 h. A: Lipid species were measured in L6 myotubes using lipidomic analysis as described in the Methods (n = 7). B: Surface GLUT4 was measured in L6-GLUT4myc myotubes as described in the Methods [n = 7; three-way ANOVA (insulin, PA, myriocin)]. C: Surface GLUT4 was measured in C2C12-GLUTmyc myotubes as described in the Methods [n = 3; three-way ANOVA (insulin, PA, myriocin)]. D, E: Expression of Ccl2 and Il6 in L6 myotubes after PA and myriocin exposure was measured by qPCR [n = 4; two-way ANOVA (PA, myriocin)]. #Overall significant effect of inhibitor (two-way ANOVA; P < 0.05; n ≥ 5). *Significant effect of PA over BSA control (two-way ANOVA; P < 0.05). §Significant effect of insulin over unstimulated control (P < 0.05). DHCer, dihydroceramide; HexCer, hexosylceramide; SPM, sphingomyelin; LacCer, lactosylceramide; MYR, myriocin.