Abstract
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.
Highlights
Obesity is caused by an increase in fat due to the imbalance of energy intake and consumption [1]
The phosphatidylinositol 3-kinase (PI3K) activator reversed these changes caused by EGCG, suggesting that the inhibitory effects of EGCG may be mediated by PI3K-protein kinase B (AKT)-Forkhead box-O1 (FOXO1) pathway to negatively regulate the expression of peroxisome proliferator activated receptor γ (PPARγ)
In order to test the effects of EGCG on glucose uptake and lipid accumulation during adipogenesis, glucose concentration test and oil red O staining were performed
Summary
Obesity is caused by an increase in fat due to the imbalance of energy intake and consumption [1]. People suffering from obesity and overweight are on a rise because of high-fat and high-calorie diets and sedentary lifestyle [2, 3]. The diseases associated with obesity include insulin resistance, fatty liver disease, type 2 diabetes, atherosclerosis, hypertension, stroke, arthritis, and numerous cancers [4, 5]. Adipose tissue can excrete a variety of bioactive polypeptides known as adipokines, including leptin, adiponectin, resistin, TNF-α, IL-6 and so on [7,8,9,10]. Adipokines regulate adipocyte differentiation, metabolism and local inflammatory reaction via autocrine and paracrine pathways, and play important roles in insulin resistance and chronic inflammation process [11, 12]
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