GTE commonly upregulated the mRNA expression level of Ppard, Rxra, Pgc1a, Ucp2, Ucp3 and Sirt1 in WAT in the OO-based HF diet-fed mice and the UFA-enriched HF diet-fed mice, suggesting that the mechanism for the effectiveness of GTE on these diet-induced fat accumulations might be due to promotion of energy expenditure through activation of PPARδ pathway in WAT and through ingestion of large amount of UFA, or PPAR ligands, into the body. The gene discussed is UCP2; the disease is hydrops fetalis.