Naringenin improved metabolic disturbances via PPARα and/or PPARγ up-regulation and stimulation (PGC1α, CPT-1, UCP1, UCP2)/suppression (LXRα, adipogenic, lipogenic) of its related underling up/downstream kinases, enzymes, genes, and receptors, thereby providing antioxidant and anti-inflammatory effects in diabetic, hypercholesterolemia, obesity, and lipid metabolism liver dysfunction models, as shown in Table 1 [109–111, 114–117]. The gene discussed is PPARGC1A; the disease is obesity due to melanocortin 4 receptor deficiency.