In addition, various rodent models have an increased susceptibility to chronic intestinal inflammation, which worsens with HFDs (11, 12), by immunological mechanisms that also resemble human IBD pathogenesis (e.g., cytokines IL-1β and TNFα, monocyte chemoattractant protein-1 (MCP1), and keratinocyte-derived chemokines) (12). This evidence concerns the gene CCL2 and inflammatory response.