Increasingly, the lipo-inflammation characteristic of MetS is considered a key complication driving health deterioration, with PPAR-α emerging as a possible link between nutrition, metabolic organs, and the immune system [8] In animal models, MetS can be induced by employing a special diet regimen, i.e., a high-fat diet (HFD), that reproduces the complete clinical manifestations in terms of increased body weight, reduced food intake, glucose tolerance, and dyslipidemia [9,10,11]. This evidence concerns the gene PPARA and metabolic syndrome.