EGCG改善高果糖饮食小鼠代谢紊乱的作用与机制研究

周继红; 陈蔚; 丁乐佳; 王岳飞

doi:10.13305/j.cnki.jts.2023.03.012

茶叶科学 >

2023 , Vol. 43 >Issue 3: 399 - 410

DOI: https://doi.org/10.13305/j.cnki.jts.2023.03.012

研究报告

EGCG改善高果糖饮食小鼠代谢紊乱的作用与机制研究

周继红 ,
陈蔚 ,
丁乐佳 ,
王岳飞

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浙江大学茶叶研究所,浙江杭州 310058

周继红,女,特聘副研究员,主要从事茶叶生物化学与人体健康研究,zhoujihong@zju.edu.cn。

收稿日期: 2022-12-12

修回日期: 2023-04-27

网络出版日期: 2023-06-29

基金资助

国家自然科学基金区域创新联合基金（U19A2034）

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Regulatory Effect and Mechanism of EGCG on Metabolic Disorders in High-fructose Diet Mice

ZHOU Jihong ,
CHEN Wei ,
DING Lejia ,
WANG Yuefei

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Tea Research Institute, Zhejiang University, Hangzhou 310058, China

Received date: 2022-12-12

Revised date: 2023-04-27

Online published: 2023-06-29

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摘要

为探究表没食子儿茶素没食子酸酯（EGCG）对高果糖饮食诱导代谢紊乱的作用功效及机制,将15只雄性SPF级C57BL/6小鼠随机分为3组：正常饮食组（NCD）、高果糖饮食组（HFD）和高果糖补充1% EGCG饮食组（HFE）。饲喂8周后测定小鼠的体质量、能量利用率、ALT和AST含量及组织形态学染色等参数。ELISA检测肝脏TNF-α、IL-1β、IL-6和肠道IL-6炎症因子水平,实时荧光定量PCR检测肝脏Srebp-1c、Tlr4、Myd88及肠道Zo-1、Tlr4、Myd88基因表达水平,免疫组化检测ZO-1、Occludin蛋白表达水平。试验表明,膳食补充EGCG能够有效抑制高果糖饮食诱导的小鼠体重增加、脂肪积累、肝脏及肠道炎症因子释放,并可上调肠壁完整性相关的Zo-1基因表达水平和ZO-1、Occludin蛋白表达水平,下调肝脏中脂质代谢相关的Srebp-1c基因表达水平,下调肠道和肝脏中炎症相关的Tlr4、Myd88基因表达水平。以上结果表明,膳食补充EGCG对高果糖饮食诱导的代谢障碍和炎症反应有一定的预防作用,其机理可能与TLR4/MyD88信号通路介导的肠-肝轴调控机制有关。

关键词： 茶多酚; 食源性肥胖; 炎症反应; 脂质代谢; 肠-肝轴

本文引用格式

周继红 , 陈蔚 , 丁乐佳 , 王岳飞 . EGCG改善高果糖饮食小鼠代谢紊乱的作用与机制研究[J]. 茶叶科学, 2023 , 43(3) : 399 -410 . DOI: 10.13305/j.cnki.jts.2023.03.012

Abstract

This study investigated the effects and mechanisms of epigallocatechin gallate (EGCG) on high-fructose diet-induced metabolic disorders. Fifteen male SPF C57BL/6 mice were randomly divided into three groups: normal diet group (NCD), high-fructose diet group (HFD), and high-fructose diet supplemented with 1% EGCG group (HFE), with 5 mice in each group. After 8 weeks of feeding, the body weight, energy utilization rate, ALT and AST levels, as well as tissue morphology staining of the mice were measured. Furthermore, hepatic TNF-α, IL-1β, IL-6 and intestinal IL-6 inflammatory cytokine levels were detected by ELISA. The expressions of Srebp-1c, Tlr4, Myd88 in liver and Zo-1, Occludin, Tlr4 and Myd88 in intestine were measured by quantitative real-time PCR. Protein expressions of ZO-1 and Occludin were detected by IHC. The results show that dietary supplementation of EGCG could effectively reduce high-fructose diet-induced body weight gain, fat accumulation, hepatic and intestinal inflammatory responses, and could improve the intestinal barrier function by upregulating the expression of Zo-1 and the protein expressions of ZO-1 and Occludin. It also modulated lipid metabolism by reducing the expression level of Srebp-1c in liver, and downregulated the expression levels of inflammatory-related genes (Tlr4 and Myd88) in colon and liver. The results above suggest that dietary supplementation of EGCG has a preventive effect on high-fructose diet-induced metabolic disorders and inflammatory responses, and its mechanism may be related to the regulation of the gut-liver axis mediated by the TLR4/MyD88 signaling pathway.

Key words： tea polyphenols; diet-induced obesity; inflammatory responses; lipid metabolism; gut-liver axis

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