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Journal of Tea Science ›› 2023, Vol. 43 ›› Issue (3): 399-410.doi: 10.13305/j.cnki.jts.2023.03.012

• Research Paper • Previous Articles     Next Articles

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

ZHOU Jihong, CHEN Wei, DING Lejia, WANG Yuefei*   

  1. Tea Research Institute, Zhejiang University, Hangzhou 310058, China
  • Received:2022-12-12 Revised:2023-04-27 Online:2023-06-15 Published:2023-06-29

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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