Experimental evidence shows that, besides being a marker of AT inflammation and dysfunction, the DPP4, per se, elicits AT remodeling under stressful conditions, such as in the condition of chronic excessive caloric intake and obesity, and its inhibition reverts inflammation in animal models [110,111,112,113,114,115,116]. This evidence concerns the gene DPP4 and obesity due to melanocortin 4 receptor deficiency.