Aged green tea reduces high-fat diet-induced fat accumulation and inflammation via activating the AMP-activated protein kinase signaling pathway
文献类型： 外文期刊
作者： Chen, Ruohong 1 ; Lai, Xingfei 1 ; Xiang, Limin 1 ; Li, Qiuhua 1 ; Sun, Lingli 1 ; Lai, Zhaoxiang 1 ; Li, Zhigang 1 ; Zhang, Wenji 1 ; Wen, Shuai 1 ; Cao, Junxi 1 ; Sun, Shili 1 ;
作者机构： 1.Guangdong Acad Agr Sci, Tea Res Inst, Guangdong Prov Key Lab Tea Plant Resources Innova, Guangzhou, Peoples R China
关键词： anti-obesity; anti-inflammation; AMPK; aged green tea; metabolism
期刊名称：FOOD & NUTRITION RESEARCH （ 影响因子：3.221； 五年影响因子：4.739 ）
ISSN： 1654-6628
年卷期： 2022 年 66 卷
页码：
收录情况： SCI
摘要： Background: Obesity is a global public health concern and increases the risk of metabolic syndrome and other diseases. The anti-obesity effects of various plant-derived bioactive compounds, such as tea extracts, are well-established. The mechanisms underlying the anti-obesity activity of Jinxuan green tea (JXGT) from different storage years are still unclear. Objective: The aim of this study was to evaluate the effects of JXGTs from three different years on the high fat diet (HFD)-fed mouse model. Design: The mice were divided into six groups, the control group received normal diet and the obese model group received HFD. We analyzed the effects of JXGTs from 2005, 2008, and 2016 on HFD-fed obese mice over a period of 7 weeks. Results: The JXGTs reduced the body weight of the obese mice, and also alleviated fat accumulation and hepatic steatosis. Mechanistically, JXGTs increased the plosplorylation of AMP-activated protein kinase (p-AMPK)/AMP-activated protein kinase (AMPK) ratio, up-regulated carnitine acyl transferase 1A (CPT-1A), and down-regulated fatty acid synthase (FAS), Glycogen synthase kinase-3beta (GSK-3 beta), Peroxisome proliferator-activated receptor-gamma co-activator-lalpha (PGC-1 alpha), Interleukin 6 (IL-6), and Tumour necrosis factor alpha (TNF alpha). Thus, JXGTs can alleviate HFD-induced obesity by inhibiting lipid biosynthesis and inflammation, thereby promoting fatty acid oxidation via the AMPK pathway. Discussion: The anti-obesity effect of three aged JXGTs were similar. However, JXGT2016 exhibited a more potent activation of AMPK, and JXGT2005 and JXGT2008 exhibited a more potent inhibiting glycogen synthase and inflammation effect. Furthermore, the polyphenol (-)-epicatechin (EC) showed the strongest positive correlation with the anti-obesity effect of JXGT. Conclusions: These findings demonstrate that JXGT treatment has a potential protection on HFD-induced obesity mice via activating the AMPK/CPT-1A and down-regulating FAS/GSK-3 beta/PGC-1 alpha and IL-6/TNF alpha. Our study results also revealed that different storage time would not affect the anti-obesity and anti-inflammation effect of JXGT.
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