Mechanisms of epigallocatechin gallate (EGCG) in ameliorating hyperuricemia: insights into gut microbiota and intestinal function in a mouse model

Epigallocatechin gallate (EGCG), a prominent bioactive compound found in tea, offers numerous health benefits. Previous studies have highlighted its potential in mitigating hyperuricemia. In this study, hyperuricemic mice induced by potassium oxonate (PO) were treated with EGCG or the anti-hyperuric...

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Veröffentlicht in:Food & function 2024-06, Vol.15 (11), p.668-681
Hauptverfasser: Yu, Haonan, Lou, Zhenyou, Wu, Tingbo, Wan, Xiaochun, Huang, Haitao, Wu, Yuanyuan, Li, Bo, Tu, Youying, He, Puming, Liu, Junsheng
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container_issue 11
container_start_page 668
container_title Food & function
container_volume 15
creator Yu, Haonan
Lou, Zhenyou
Wu, Tingbo
Wan, Xiaochun
Huang, Haitao
Wu, Yuanyuan
Li, Bo
Tu, Youying
He, Puming
Liu, Junsheng
description Epigallocatechin gallate (EGCG), a prominent bioactive compound found in tea, offers numerous health benefits. Previous studies have highlighted its potential in mitigating hyperuricemia. In this study, hyperuricemic mice induced by potassium oxonate (PO) were treated with EGCG or the anti-hyperuricemia medication allopurinol (AP) to investigate the mechanisms underlying their anti-hyperuricemic effects. The results demonstrated that both EGCG and AP significantly reduced serum uric acid (UA) levels. Further analysis revealed that EGCG promoted the expression of UA secretion transporter genes ( Oat1 and Oct1 ) while inhibiting the expression of UA reabsorption transporter genes ( Urat1 and Glut9 ) in the kidney. By 16S rDNA sequencing, EGCG, but not AP, was found to alter the composition of the gut microbiota. Notably, EGCG induced significant changes in the relative abundance of specific bacteria such as Lactobacillus , Faecalibaculum , and Bifidobacterium , which displayed high correlations with serum UA levels and UA-related gene expression. Metabolomic analysis suggested that EGCG-induced modifications in bacterial metabolites might contribute to the alleviation of hyperuricemia. Transcriptomic analysis of the intestinal epithelium identifies 191 differentially expressed genes (DEGs) in EGCG-treated mice, including 8 purine-related genes. This study elucidates the anti-hyperuricemic mechanisms of EGCG, particularly its influence on the gut microbiota and gene expression in the intestinal epithelium. Epigallocatechin gallate (EGCG), a prominent bioactive compound found in tea, offers numerous health benefits.
doi_str_mv 10.1039/d4fo01606h
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Previous studies have highlighted its potential in mitigating hyperuricemia. In this study, hyperuricemic mice induced by potassium oxonate (PO) were treated with EGCG or the anti-hyperuricemia medication allopurinol (AP) to investigate the mechanisms underlying their anti-hyperuricemic effects. The results demonstrated that both EGCG and AP significantly reduced serum uric acid (UA) levels. Further analysis revealed that EGCG promoted the expression of UA secretion transporter genes ( Oat1 and Oct1 ) while inhibiting the expression of UA reabsorption transporter genes ( Urat1 and Glut9 ) in the kidney. By 16S rDNA sequencing, EGCG, but not AP, was found to alter the composition of the gut microbiota. Notably, EGCG induced significant changes in the relative abundance of specific bacteria such as Lactobacillus , Faecalibaculum , and Bifidobacterium , which displayed high correlations with serum UA levels and UA-related gene expression. Metabolomic analysis suggested that EGCG-induced modifications in bacterial metabolites might contribute to the alleviation of hyperuricemia. Transcriptomic analysis of the intestinal epithelium identifies 191 differentially expressed genes (DEGs) in EGCG-treated mice, including 8 purine-related genes. This study elucidates the anti-hyperuricemic mechanisms of EGCG, particularly its influence on the gut microbiota and gene expression in the intestinal epithelium. 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Metabolomic analysis suggested that EGCG-induced modifications in bacterial metabolites might contribute to the alleviation of hyperuricemia. Transcriptomic analysis of the intestinal epithelium identifies 191 differentially expressed genes (DEGs) in EGCG-treated mice, including 8 purine-related genes. This study elucidates the anti-hyperuricemic mechanisms of EGCG, particularly its influence on the gut microbiota and gene expression in the intestinal epithelium. 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Previous studies have highlighted its potential in mitigating hyperuricemia. In this study, hyperuricemic mice induced by potassium oxonate (PO) were treated with EGCG or the anti-hyperuricemia medication allopurinol (AP) to investigate the mechanisms underlying their anti-hyperuricemic effects. The results demonstrated that both EGCG and AP significantly reduced serum uric acid (UA) levels. Further analysis revealed that EGCG promoted the expression of UA secretion transporter genes ( Oat1 and Oct1 ) while inhibiting the expression of UA reabsorption transporter genes ( Urat1 and Glut9 ) in the kidney. By 16S rDNA sequencing, EGCG, but not AP, was found to alter the composition of the gut microbiota. Notably, EGCG induced significant changes in the relative abundance of specific bacteria such as Lactobacillus , Faecalibaculum , and Bifidobacterium , which displayed high correlations with serum UA levels and UA-related gene expression. Metabolomic analysis suggested that EGCG-induced modifications in bacterial metabolites might contribute to the alleviation of hyperuricemia. Transcriptomic analysis of the intestinal epithelium identifies 191 differentially expressed genes (DEGs) in EGCG-treated mice, including 8 purine-related genes. This study elucidates the anti-hyperuricemic mechanisms of EGCG, particularly its influence on the gut microbiota and gene expression in the intestinal epithelium. Epigallocatechin gallate (EGCG), a prominent bioactive compound found in tea, offers numerous health benefits.</abstract><cop>England</cop><pub>Royal Society of Chemistry</pub><pmid>38757391</pmid><doi>10.1039/d4fo01606h</doi><tpages>14</tpages><orcidid>https://orcid.org/0000-0002-7294-6888</orcidid><orcidid>https://orcid.org/0000-0003-2481-4415</orcidid><orcidid>https://orcid.org/0000-0002-9539-1678</orcidid></addata></record>
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source MEDLINE; Royal Society Of Chemistry Journals 2008-
subjects Allopurinol
Allopurinol - pharmacology
Animals
Bacteria
Bacteria - classification
Bacteria - drug effects
Bacteria - genetics
Bacteria - isolation & purification
Bioactive compounds
Catechin - analogs & derivatives
Catechin - pharmacology
Digestive system
Disease Models, Animal
Epigallocatechin gallate
Epithelium
Gastrointestinal Microbiome - drug effects
Gastrointestinal tract
Gene expression
Genes
Glucose Transport Proteins, Facilitative
Hyperuricemia
Hyperuricemia - drug therapy
Intestinal microflora
Intestine
Intestines - drug effects
Intestines - microbiology
Kidney - drug effects
Kidney - metabolism
Male
Metabolites
Metabolomics
Mice
Mice, Inbred C57BL
Microbiota
Microorganisms
Organic Anion Transporters - genetics
Organic Anion Transporters - metabolism
Oxonic Acid
Reabsorption
Relative abundance
rRNA 16S
Transcriptomics
Uric acid
Uric Acid - blood
Uric Acid - metabolism
title Mechanisms of epigallocatechin gallate (EGCG) in ameliorating hyperuricemia: insights into gut microbiota and intestinal function in a mouse model
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