Graduate School of Life and Environmental Sciences, University of Tsukuba, Ibaraki, Japan.
Cell Biol Int. 2012 Feb;36(2):147-53. doi: 10.1042/CBI20110047.
EGCG [(-)-epigallocatechin gallate], tea catechin, is one of the compounds that has been reported to act against obesity and diabetes. To determine the effect of EGCG on adipocyte differentiation, we treated 3T3-L1 preadipocytes with different catechins. Oil Red O staining showed significantly reduced intracellular lipid accumulation, especially with EGCG. Cell cycle analysis showed that EGCG inhibited cell proliferation by disturbing the cell cycle during the clonal expansion of 3T3-L1. RT-PCR (real-time PCR) demonstrated that EGCG noticeably reduced mRNA expression of PPARγ (peroxisome proliferator-activated receptor γ), C/EBPα (CCAAT/enhancer-binding protein α) and FoxO1 (forkhead box class O1). EGCG also caused a significant decrease in the transcription of FoxO1 - the forkhead transcription factor class O1 involved in adipocyte differentiation - via the PI3K (phosphoinositide 3-kinase)/Akt and MEK [MAPK (mitogen-activated protein kinase)/ERK (extracellular-signal-regulated kinase) kinase] pathways. These results suggest that EGCG suppresses the clonal expansion of adipocytes by inactivating FoxO1 via insulin signalling and stress-dependent MAPK pathways.
EGCG（(-)-表没食子儿茶素没食子酸酯），茶儿茶素，是一种据报道可对抗肥胖和糖尿病的化合物。为了确定 EGCG 对脂肪细胞分化的影响，我们用不同的儿茶素来处理 3T3-L1 前脂肪细胞。油红 O 染色显示细胞内脂质积累明显减少，尤其是 EGCG。细胞周期分析表明，EGCG 通过干扰 3T3-L1 克隆扩张过程中的细胞周期来抑制细胞增殖。RT-PCR（实时 PCR）表明，EGCG 显著降低了过氧化物酶体增殖物激活受体 γ（PPARγ）、CCAAT/增强子结合蛋白 α（C/EBPα）和叉头框 O1（FoxO1）的 mRNA 表达。EGCG 还通过 PI3K（磷酸肌醇 3-激酶）/Akt 和 MEK [MAPK（丝裂原激活蛋白激酶）/ERK（细胞外信号调节激酶）激酶]途径，导致 FoxO1 的转录显著减少，FoxO1 是参与脂肪细胞分化的叉头转录因子 O1 家族的一员。这些结果表明，EGCG 通过胰岛素信号和应激依赖的 MAPK 途径使 FoxO1 失活，从而抑制脂肪细胞的克隆扩张。
