Peroxisome proliferator-activated receptors as targets to treat non-alcoholic fatty liver disease

Figure 1 Effects of each peroxisome proliferator-activated receptor isoform in the treatment of non-alcoholic fatty liver disease. PPAR-alpha activation leads to the transcription of CPT-1, a target gene that is crucial to beta-oxidation as it allows the fatty acid to reach the mitochondrial matrix; PPAR-beta/delta activation is involved with FOXO-1 transcription, which reduces the hepatic expression of enzymes involved in gluconeogenesis. Thus, GLUT2 and hepatic glucose production are also significantly reduced; conversely, the partial activation of PPAR-gamma or, even, its reduced expression is linked to diminished lipogenesis. All these events are efficient to tackle NAFLD. PPAR: Peroxisome proliferator-activated receptor; CPT-1: Carnitine palmitoyl transferase-1; FOXO-1: Forkhead box-containing protein O subfamily-1; GLUT2: Glucose transporter 2; SREBP-1c: Sterol regulatory element-binding protein-1c.