The toll like receptor 4 (TLR4) recognizes endogenous free fat acid and exogenous pathogens [20], [21] and engagement of TLR4 activates the nuclear factor κB (NF-κB) [22] and mitogen-activated protein kinase (MAPK) subfamily members [23], including the extracellular-signal-regulated kinase (ERK), c-Jun N-terminal kinases (JNK) and p38 MAPK, as well ascytokines [24], and stimulates the production of inflammatory cytokines, such as tumor necrosis factor (TNF)-α and interleukin (IL)-6, contributing to glucose intolerance and insulin resistance. This evidence concerns the gene IL6 and Insulin resistance.