“…The activation of AMPK modulates the expression of genes and proteins involved in lipid metabolism, downregulates the expression of fat synthesis proteins, and upregulates lipid catabolism proteins [ 2 ]. It was shown that EGCG inhibited the expressions of glucose 6-phosphatase (G6Pase, for gluconeogenesis), phosphoenolpyruvate carboxykinase, (PEPCK, for gluconeogenesis), fatty acid synthase (FAS, for fatty acid synthesis), acetyl-CoA carboxylase (ACC, for fatty acid synthesis), hydroxymethylglutaryl-CoA reductase (HMGR, for cholesterol), sterol regulatory element-binding proteins (SREBPs, for sterol synthesis), peroxisome proliferator-activated receptor gamma (PPAR γ , for lipid synthesis and storage), and CCAAT/enhancer-binding protein alpha (C/EBP α , for adipogenesis) as well as enhanced the expression of acyl-CoA oxidase (ACO, for fatty acid oxidation), peroxisome proliferator-activated receptor alpha (PPAR α , for fatty acid oxidation), carnitine palmitoyltransferase-1 (CPT-1, for fatty acid oxidation), acyl-CoA dehydrogenase (ACAD, for fatty acid oxidation), peroxisome proliferator-activated receptor gamma coactivator-1 α (PGC-1 α , for fatty acid oxidation), uncoupling proteins (UCPs, for thermogenesis), and adipose triglyceride lipase (ATGL, for triglyceride hydrolysis) [ 50 – 54 ].…”