While peripheral tissues develop a significant insulin resistance during the course of sepsis due to the downregulation of GLUT4 [35] and the impairment of post-receptor signaling pathways (via the phosphorylation of the insulin receptor, insulin receptor substrate 1 (IRS-1) and MAP kinase) [36], GLUT1 seems to be upregulated in brain cells of mice following thermal injury or infection with Pseudomonas aeruginosa, [37]. This evidence concerns the gene IRS1 and Insulin resistance.