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ABSTRACT Epigallocatechin‐3‐gallate (EGCG), a major component in green tea, functions as extensive bioactivities including anti‐inflammation, anti‐oxidation, and anti‐cancer. However, little is known about its anti‐adipogenesis and underlying mechanisms. The purport of this study sought to investigate effects of EGCG on 3T3‐L1 preadipocyte differentiation and to explore its possible mechanisms. The 3T3‐L1 cells were induced to differentiate under the condition of pro‐adipogenic cocktail with or without indicated EGCG concentrations (10, 50, 100, 200 &mgr;M) for 2, 4, 6 and 8 days, respectively. Also, another batch of 3T3‐L1 cells was induced under the optimal EGCG concentration (100 &mgr;M) with or without SC3036 (PI3K activator, 10 &mgr;M) or SC79 (AKT activator, 0.5 &mgr;M) for 8 days. Subsequently, the cell viability was examined by MTT assay and the cell morphology was visualized by Oil red O staining. Finally, the mRNA levels including peroxisome proliferator activated receptor &ggr; (PPAR&ggr;) and fatty acid synthase (FAS) were detected by quantitative real time PCR, while the protein levels of PPAR&ggr;, FAS, phosphatidylinositol 3 kinase (PI3K), insulin receptor substrate1(IRS1), AKT, and p‐AKT were measured by immunoblotting analysis. Our results showed that EGCG inhibited adipogenesis of 3T3‐L1 preadipocyte in a concentration‐dependent manner. Moreover, the inhibitory effects were reversed by SC3036 or SC79, suggesting that the inhibitory effects of EGCG are mediated by PI3K‐AKT signaling to down‐regulate PPAR&ggr; and FAS expression levels. The findings shed light on EGCG anti‐adipogenic effects and its underlying mechanism and provide a novel preventive‐therapeutic potential for obesity subjects as a compound from Chinese green tea. Graphical abstract Figure. No Caption available.