SLC2A4 and Insulin resistance: In vitro data also support the involvement of LPSs in the pathogenesis of insulin resistance, with evidence for the disruption of the insulin signaling pathway via the phosphorylation of JNK and a reduction in the insulin-induced phosphorylation of IRS-1 on the tyrosine residue, Akt and AS160 proteins implicated in GLUT4 translocation to the plasma membrane and glucose uptake [152,153,154].