Such inflammatory or M1-like macrophages were thought to elaborate proinflammatory mediators (e.g., tumor necrosis factor alpha; TNF-α [18], interleukin-1 beta; IL-1β [19,20], monocyte chemoattractant protein; MCP-1/CCL2 [12], and bioactive lipid mediators (e.g., prostaglandins and leukotrienes [21]) that potentiated local and systemic inflammation, and ultimately, insulin resistance. This evidence concerns the gene TNF and Insulin resistance.