The anti-obesity prospective of green tea catechins, especially EGCG, has been shown in cell culture, animal and human research. Table 1 lists the in vitro activities of EGCG and green tea extracts (GTE) in inhibiting preadipocyte differentiation, decreasing adipocyte proliferation, inducing adipocyte apoptosis, suppressing lipogenesis, and advertising lipolysis and fatty acid beta ()-oxidation [178]. EGCG (1000 ) and with reduce potencies, EC and EGC, induce dose- and timedependent reduce in adipocyte viability [28, 29] and cell cycle arrest in the G0/G1 phase [19]. At reduce concentrations (00 ) EGCG induced G2/M growth arrest in a dosedependent manner in mature 3T3-L1 adipocytes [17]. Concurrently, EGCG (000 ) and much less potently ECG, EGC and also other catechins induce apoptosis in murine 3T3-L1 preadipocyte [29] and mature 3T3-L1 adipocytes [26] as shown by DNA fragmentation [29] and improved caspase-3 activity [29]. In addition, EGCG (0.50 ) inhibits preadipocyte differentiation and at greater concentrations (5000 ) [17, 21, 24, 26, 28], cellular triglyceride accumulation in adipocytes in a dose- and time-dependent manner. EGCG-mediated suppression of adipocyte differentiation may possibly be attributed to its impact on genes playing vital roles in adipocyte differentiation (Figure 1). Peroxisome proliferator activator receptor (PPAR) and CCAAT/enhancer binding protein (C/EBP) are two important regulators of adipocyte differentiation that orchestrate the expression of adipogenic and lipogenic genes; these genes contain acetyl-coenzyme A carboxylase (ACC) that converts acetyl-CoA to malonyl-CoA, a constructing block for fatty acid synthesis and an inhibitor for fatty acid oxidation [30], along with the transcriptional factor sterol regulatory element-binding protein 1c (SREBP-1c) that enhances lipogenesis and adipogenesis [21]. EGCG’s impact on adipocyte differentiation is accompanied by down-regulation in the expression of PPAR and C/EBP at the mRNA and protein levels [17] and activation of AMP-activated protein kinase (AMPK), a suppressor of PPAR and C/EBP expression [17, 20]. Complementing EGCG’s effect on adipocyte differentiation is EGCG’s ability to upregulate lipolysis and thermogenesis [24]. EGCG was identified to improve glycerol release plus the expression of hormone sensitive lipase and carnitine palmitoyltransferase-1 (CPT-1) that may be involved in fatty acid -oxidation in 3T3-L1 cells [17].Nootkatone Epigenetic Reader Domain The mRNA levels of uncouplingJ Nutr Biochem.Diethyl Formula Author manuscript; available in PMC 2015 January 01.PMID:23329319 Wang et al.Pageprotein (UCP)-2, a crucial protein in fat-supported thermogenesis, was increased by EGCG (010 ) in a dose-dependent manner [25].NIH-PA Author Manuscript NIH-PA Author Manuscript NIH-PA Author ManuscriptIn addition to the effects of EGCG described above, decreased expression of resistin [27], an adipocyte-derived inflammatory adipokine that’s associated with insulin resistance and enhanced threat of cardiovascular disease (CVD) [31], may possibly also contribute for the EGCGmediated anti-inflammatory response [31] and insulin sensitization [24, 25, 27]. In 3T3-L1 adipocytes, incubation with 100 EGCG for three hours decreased both mRNA and protein levels of resistin by 50 [27]. Preclinical research in animals [324] additional confirmed the valuable effects of EGCG or GTE on obesity-related parameters such as decreased BW [34, 35, 37, 39, 425, 474], adipose mass [325, 37, 392, 44, 45, 47, 504], total lipids, cholesterol, triglyceride (TG), and triacylglycerol (TAG) in liver.