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茶儿茶素抑制3T3-L1细胞中的脂肪细胞分化,同时伴随着过氧化物酶体增殖物激活受体γ2(PPARγ2)和CCAAT/增强子结合蛋白α(C/EBPα)的下调。

Tea catechin suppresses adipocyte differentiation accompanied by down-regulation of PPARgamma2 and C/EBPalpha in 3T3-L1 cells.

作者信息

Furuyashiki Takashi, Nagayasu Hironobu, Aoki Yukiko, Bessho Hiroaki, Hashimoto Takashi, Kanazawa Kazuki, Ashida Hitoshi

机构信息

Department of Biofunctional Chemistry, Graduate School of Science and Technology, Kobe University, Japan.

出版信息

Biosci Biotechnol Biochem. 2004 Nov;68(11):2353-9. doi: 10.1271/bbb.68.2353.

Abstract

Obesity is a serious health problem, and its prevention is promoted through life style including diet and exercise. In this study, we investigated the suppressive effects of tea catechin on the differentiation of 3T3-L1 preadipocytes to adipocytes. (-)-Catechin 3-gallate (CG), (-)-epigallocatechin (EGC), (-)-epicatechin 3-gallate, and (-)-epigallocatechin 3-gallate at 5 muM suppressed intracellular lipid accumulation. The suppressive effects of CG and EGC were stronger than the others, and CG and EGC also suppressed the activity of glycerol-3-phosphate dehydrogenase as a differentiation marker. These catechins inhibited the expression of peroxisome proliferator-activated receptor (PPAR) gamma2 and CCAAT/enhancer-binding protein (C/EBP) alpha, both of which act as key transcription factors at an early stage of differentiation, followed by the expression of glucose transporter (GLUT) 4 at a later stage. In addition, the catechins did not affect the phosphorylation status of the insulin signal pathway. Thus, catechin suppressed adipocyte differentiation accompanied by the down-regulation of PPARgamma2, C/EBPalpha, and GLUT4. These results suggest that tea catechin prevents obesity through the suppression of adipocyte differentiation.

摘要

肥胖是一个严重的健康问题,可通过包括饮食和运动在内的生活方式来促进其预防。在本研究中,我们调查了茶儿茶素对3T3-L1前脂肪细胞向脂肪细胞分化的抑制作用。5 μM的(-)-儿茶素3-没食子酸酯(CG)、(-)-表没食子儿茶素(EGC)、(-)-表儿茶素3-没食子酸酯和(-)-表没食子儿茶素3-没食子酸酯可抑制细胞内脂质积累。CG和EGC的抑制作用比其他儿茶素更强,并且CG和EGC还抑制了作为分化标志物的甘油-3-磷酸脱氢酶的活性。这些儿茶素抑制了过氧化物酶体增殖物激活受体(PPAR)γ2和CCAAT/增强子结合蛋白(C/EBP)α的表达,这两种蛋白在分化早期均作为关键转录因子发挥作用,随后在后期抑制了葡萄糖转运蛋白(GLUT)4的表达。此外,儿茶素不影响胰岛素信号通路的磷酸化状态。因此,儿茶素通过下调PPARγ2、C/EBPα和GLUT4来抑制脂肪细胞分化。这些结果表明,茶儿茶素通过抑制脂肪细胞分化来预防肥胖。

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