Epigallocatechin-3-gallate suppresses differentiation of adipocytes via regulating the phosphorylation of FOXO1 mediated by PI3K-AKT signaling in 3T3-L1 cells
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Yi Lu1,2,*, Junye Chen3,4,*, Tao Xian1,2,*, Yumeng Zhou1,2, Wanwan Yuan1,2, Mengxi Wang1,2, Yuyang Gan3,4, Kun Wang1,2, Shaofeng Xiong1,2, Cong Ma3, Xueying Yu3 and Qiren Huang1,2
1Key Provincial Laboratory of Basic Pharmacology, Nanchang University, Nanchang 330006, Jiangxi Province, P.R. China
2Department of Pharmacology, School of Pharmacy, Nanchang University, Nanchang 330006, Jiangxi Province, P.R. China
3Jiangxi Medical School, Nanchang University, Nanchang 330006, Jiangxi Province, P.R. China
4Nanchang Joint Programme, Queen Mary University of London, London E1 4NS, UK
*These authors contributed equally to this work
Qiren Huang, email: [email protected]
Keywords: epigallocatechin-3-gallate; adipogenesis; adipocyte; forkhead box-O1; peroxisome proliferator activated receptor γ
Received: August 30, 2017 Accepted: December 04, 2017 Published: December 21, 2017
Epigallocatechin-3-gallate (EGCG) is a pivotal effective component of green tea. It is known that EGCG has antioxidant activity, anti-angiogenesis, anti-tumor, cardiovascular protection and blood lipid regulation functions. Forkhead box-O1 (FOXO1) is one of the downstream signals of protein kinase B (AKT) and takes part in adipogenesis. The purpose of this study is to investigate the effects of EGCG on adipose differentiation and the likely mechanisms. 3T3-L1 cells were induced by DMI for 2, 4, 6 and 8 days, respectively. During induction, the cells were treated with EGCG (5 μM, 10 μM, 50 μM and 100 μM) or DMSO for the first 2 days. In addition, another batch of 3T3-L1cells were treated with SC-3036 (PI3K activator, 10 μM), or LY294002 (PI3K inhibitor, 10 μM) alone or combined with EGCG (100 μM) for the indicated times. Medium glucose concentration, lipid accumulation, the levels of TNF-α, resistin, adiponectin and leptin and the expression of FOXO1, phosphorylated-FOXO1 (P-FOXO1), PPARγ, fatty acid synthase (FAS) were detected, respectively. The present study demonstrated that EGCG inhibited glucose uptake, lipid accumulation and adipokine secretion in a concentration-dependent manner during adipogenesis, which suggests that EGCG inhibits adipocyte’s differentiation, maturation and functions. Moreover, EGCG also down-regulated the expression levels of PPARγ and P-FOXO1. Conversely, the PI3K activator reversed these changes caused by EGCG, suggesting that the inhibitory effects of EGCG may be mediated by PI3K-AKT-FOXO1 pathway to negatively regulate the expression of PPARγ. The findings will provide a solid foundation for EGCG to prevent and cure the obesity-associated diseases.
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