See related article, pages 80–88 Peroxisome proliferator-activated receptors (PPARs) are ligand-inducible transcription factors that belong to the nuclear hormone receptor superfamily.1 In mammals, the PPAR family consists of 3 subtypes of proteins encoded by separate genes: PPARα (NR1C1), PPARγ (NR1C3), and PPARδ (also known as β or NR1C2).2 They act as heterodimers with the retinoid X receptor and regulate gene transcription by binding to specific response elements in the promoter of the target genes.3 The classical biological activity of PPARα is the regulation of the rate of fatty acid uptake and their esterification into triglyceride or oxidation,4–7 whereas PPARγ is classically involved in adipocyte differentiation, regulation of fat storage, and maintenance of glucose homeostasis.5 The physiological functions of PPARδ are instead still unclear, although it is known that this receptor contributes to an inflammatory switch through its association and disassociation with transcriptional repressors.8 The clinical importance of PPARs originates with fibrates and thiazolidinediones (TZDs), which respectively act on PPARα and PPARγ and are used to ameliorate hyperlipidemia and hyperglycemia in subjects with type 2 diabetes mellitus (T2DM). Fibrates, such as gemfibrozil, clofibrate, fenofibrate, and bezofibrate, are drugs that effectively reduce triglycerides (TG) and free …