Our results suggest that EEP attenuates hyperthyroidism-induced oxidative stress via the PPAR and AMPK pathways, with the main targets of action being by influencing the expression of FABP and HMGCR at the protein level and by affecting the expression of EHHADH, HMGCR, and SLC27A2 at the mRNA level. This evidence concerns the gene EHHADH and hyperthyroidism.