Also, hindering pro-inflammatory pathways triggered by Toll-like receptor-LPS (TLR-LPS) and prohibiting Toll-like-receptor-4 (TLR4) activation (28, 29), decreasing inflammatory cytokine production and consequently reducing hepatic triglyceride synthesis through attenuating insulin resistance (29), are reported as potential mechanisms. This evidence concerns the gene TLR4 and Insulin resistance.