Several studies have proposed that the central mechanism underlying obesity and its related comorbidities comes from a persistent state of low-grade chronic inflammation together with dysregulation in the inflammation-stress feedback mechanisms (4–6), mainly due to increased production of pro-inflammatory markers such as leptin, interleukin-6 (IL-6), tumor necrosis factor -α (TNF-α), C-reactive protein (CRP) and monocyte chemotactic protein - 1 (MCP1) in the withe adipose tissue, together with the M1 macrophage phenotype infiltration in this tissue associated with obesity (6–8). This evidence concerns the gene CCL2 and Obesity.