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Postulated interaction between the insulin signaling pathway and activation of the pro-inflammatory cascade in the pathogenesis of insulin resistance in sepsis. GLUT, glucose transporter; IκB, inhibitor κB; IKK, inhibitor κB kinase; IRS-1, insulin receptor substrate-1; LBP, lipopolysaccharide binding protein; LPS, lipopolysaccharide; NF-κB, nuclear factor-kappa B; NO, nitric oxide; TLR4, Toll-like receptor-4.
