Both bacterial components such as lipopolysaccharide (LPS), and proinflammatory cytokines such as interleukin (IL)-1β, IL-6, and tumor necrosis factor (TNF)-α, resulting from the immune response to sepsis, may activate intracellular mechanisms associated with insulin resistance, such as the IKKβ/NF-κB, and JNK pathways. This evidence concerns the gene IL1B and Sepsis.