Using selective inhibitors in animal models of obesity and in cultured adipocytes, AT COX-2 and its downstream product PGE2 have been seen to contribute in mediating inflammation in visceral fat (increased NF-κB activity, MCP-1, TNF-α, leptin and ROS production, macrophage infiltration and decreased adiponectin) accompanied by the development of systemic IR and fatty liver [88,89]. This evidence concerns the gene NFKB1 and obesity disorder.