Effects of DMH1 on the phosphorylation of Akt.

<p>(<b>A</b>) DMH1 activated Akt in L6 cells. L6 cells were treated with 1 µM, 5 µM and 10 µM DMH1 for 24 hrs. n = 5. *<i>P</i><0.05, **<i>P</i><0.01 vs controls. (<b>B</b>) Akt inhibitor inhibited DMH1-induced Akt activation. L6 cells were preincubated with 0.5 µM Akt inhibitor for 1 hr before incubated with 10 µM DMH1 for 24 hrs. Whole cell lysate was detected for p-Akt through immunoblotting. n = 6. **<i>P</i><0.01 vs control. ##<i>P</i><0.01 vs DMH1. The concentration of insulin was 100 nM, and the incubation period was 30 min. (<b>C–E</b>) Akt inhibitor (0.5 µM) inhibited DMH1(10 µM)-induced glucose consumption, glucose uptake, and lactic acid release in L6 cells. **<i>P</i><0.01 vs control. #<i>P</i><0.05, ##<i>P</i><0.01 vs DMH1. (<b>F–H</b>) Akt inhibitor (0.5 µM) alone showed no significant effects on glucose consumption and lactic acid release, but inhibited p-Akt level in L6 cells. Akti, Akt1/2 kinase inhibitor, (1,3-Dihydro-1-(1-((4-(6-phenyl-1H -imidazo[4,5-g]quinoxalin-7-yl)phenyl)methyl)-4-piperidinyl)-2H-benzimidazol-2-one trifluoroacetate salt hydrate). **<i>P</i><0.01 vs control. (<b>I</b>) Akt siRNA inhibited DMH1-induced increase of glucose consumption in L6 cells. **<i>P</i><0.01 vs control. #<i>P</i><0.05, vs DMH1+NC. NC, negative control.