JAK-STAT signaling pathway is integrated with insulin signalisation. JAK inhibition by competitive ATP inhibitors Ruxolitinib and Tofacitinib could influence the activation of insulin signaling pathways PI3K/Akt/AS160 and MEK/ERK. Interleukin-6 also influences the insulin signalisation by inhibiting IRS and blocking the signal transduction inside the cell. Chronic inhibition can lead to insulin resistance, especially in skeletal muscle cells which have a very high glucose consumption. High concentration of STAT3 is linked to insulin resisatance and type 2 diabetes. We wandered how JAK inhibitors influence the responsivnes of Akt, AS160 and Erk1/2 on insulin stimulation. We also wanted to know how interleukin-6 in high concentrarion influences the same proteins. We compared the phosphorilation of Akt, AS160 and Erk1/2 in basal conditions, with insulin and with JAK inhibitor. We also compared phosphorilation of the same proteins with the addition of interleukin-6, insulin and JAK inhibitors. The experiments were preformed on L6 myotubes and western blotting was used for protein phosphorilation analasys. We confirmed that Ruxolitinib increases the responsivnes of skeletal muscle cells on insulin signalisation in basal conditions. With the addition of high concentration of interleukin-6 Ruxolitinib and Tofacitinib slightly increased the activation of Akt/AS160 signaling pathway, but did not influence the Erk1/2 signaling pathway.
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