IGF1 and Sepsis: The ability of sepsis and LPS from the cell wall of gram-negative bacteria to stimulate the local and systemic production of inflammatory mediators [tumor necrosis factor-alpha (TNFα), interleukin (IL)-6, nitric oxide synthase (NOS)-2] and/or reduce anabolic stimuli [e.g., insulin-like growth factor (IGF)-I] appears central to mTOR inhibition [9], [15]–[19].