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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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 |
format | Article |
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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.</description><identifier>ISSN: 2042-6496</identifier><identifier>EISSN: 2042-650X</identifier><identifier>DOI: 10.1039/d4fo01606h</identifier><identifier>PMID: 38757391</identifier><language>eng</language><publisher>England: Royal Society of Chemistry</publisher><subject>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</subject><ispartof>Food & function, 2024-06, Vol.15 (11), p.668-681</ispartof><rights>Copyright Royal Society of Chemistry 2024</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c296t-fca6c9d08f2c2a06efa5bce07d248fcb5d1f719ab4532d2e3facff2ebe8d53f33</cites><orcidid>0000-0002-7294-6888 ; 0000-0003-2481-4415 ; 0000-0002-9539-1678</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/38757391$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Yu, Haonan</creatorcontrib><creatorcontrib>Lou, Zhenyou</creatorcontrib><creatorcontrib>Wu, Tingbo</creatorcontrib><creatorcontrib>Wan, Xiaochun</creatorcontrib><creatorcontrib>Huang, Haitao</creatorcontrib><creatorcontrib>Wu, Yuanyuan</creatorcontrib><creatorcontrib>Li, Bo</creatorcontrib><creatorcontrib>Tu, Youying</creatorcontrib><creatorcontrib>He, Puming</creatorcontrib><creatorcontrib>Liu, Junsheng</creatorcontrib><title>Mechanisms of epigallocatechin gallate (EGCG) in ameliorating hyperuricemia: insights into gut microbiota and intestinal function in a mouse model</title><title>Food & function</title><addtitle>Food Funct</addtitle><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.</description><subject>Allopurinol</subject><subject>Allopurinol - pharmacology</subject><subject>Animals</subject><subject>Bacteria</subject><subject>Bacteria - classification</subject><subject>Bacteria - drug effects</subject><subject>Bacteria - genetics</subject><subject>Bacteria - isolation & purification</subject><subject>Bioactive compounds</subject><subject>Catechin - analogs & derivatives</subject><subject>Catechin - pharmacology</subject><subject>Digestive system</subject><subject>Disease Models, Animal</subject><subject>Epigallocatechin gallate</subject><subject>Epithelium</subject><subject>Gastrointestinal Microbiome - drug effects</subject><subject>Gastrointestinal tract</subject><subject>Gene expression</subject><subject>Genes</subject><subject>Glucose Transport Proteins, Facilitative</subject><subject>Hyperuricemia</subject><subject>Hyperuricemia - drug therapy</subject><subject>Intestinal microflora</subject><subject>Intestine</subject><subject>Intestines - drug effects</subject><subject>Intestines - microbiology</subject><subject>Kidney - drug effects</subject><subject>Kidney - metabolism</subject><subject>Male</subject><subject>Metabolites</subject><subject>Metabolomics</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Microbiota</subject><subject>Microorganisms</subject><subject>Organic Anion Transporters - genetics</subject><subject>Organic Anion Transporters - metabolism</subject><subject>Oxonic Acid</subject><subject>Reabsorption</subject><subject>Relative abundance</subject><subject>rRNA 16S</subject><subject>Transcriptomics</subject><subject>Uric acid</subject><subject>Uric Acid - blood</subject><subject>Uric Acid - metabolism</subject><issn>2042-6496</issn><issn>2042-650X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2024</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpdkcFOGzEQhq2qqEGUS--tLPUClUK9ttdZ91YFCEigXIrEbeW1x4mj3XVq7x54DZ6YCQlUqg_2eOab0fz6CflSsIuCCf3TSR9ZoZhafyDHnEk-VSV7_PgWS60m5DTnDcMjtK509YlMRDUrZ0IXx-T5Huza9CF3mUZPYRtWpm2jNQPmQ093P4zp2dVivjinmDEdtCEmM4R-RddPW0hjCha6YH5hOYfVesgYDJGuxoF2wabYhDgYanq3y0PGTtNSP_Z2CLF_nUm7OGbA20H7mRx502Y4Pbwn5OH66s_8Znq3XNzOf99NLddqmHprlNWOVZ5bbpgCb8rGAps5Litvm9IVflZo08hScMdBeGO959BA5UrhhTghZ_u52xT_jrhW3YVsAfX2gNvUgpVKKSEqiej3_9BNHBOq2FFKFrwqpUbqx55CyTkn8PU2hc6kp7pg9c6s-lJeL1_NukH422Hk2HTg3tE3axD4ugdStu_Vf26LF2z8nGI</recordid><startdate>20240604</startdate><enddate>20240604</enddate><creator>Yu, Haonan</creator><creator>Lou, Zhenyou</creator><creator>Wu, Tingbo</creator><creator>Wan, Xiaochun</creator><creator>Huang, Haitao</creator><creator>Wu, Yuanyuan</creator><creator>Li, Bo</creator><creator>Tu, Youying</creator><creator>He, Puming</creator><creator>Liu, Junsheng</creator><general>Royal Society of Chemistry</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7T5</scope><scope>7T7</scope><scope>7TO</scope><scope>7U7</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>P64</scope><scope>7X8</scope><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></search><sort><creationdate>20240604</creationdate><title>Mechanisms of epigallocatechin gallate (EGCG) in ameliorating hyperuricemia: insights into gut microbiota and intestinal function in a mouse model</title><author>Yu, Haonan ; Lou, Zhenyou ; Wu, Tingbo ; Wan, Xiaochun ; Huang, Haitao ; Wu, Yuanyuan ; Li, Bo ; Tu, Youying ; He, Puming ; Liu, Junsheng</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c296t-fca6c9d08f2c2a06efa5bce07d248fcb5d1f719ab4532d2e3facff2ebe8d53f33</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2024</creationdate><topic>Allopurinol</topic><topic>Allopurinol - pharmacology</topic><topic>Animals</topic><topic>Bacteria</topic><topic>Bacteria - classification</topic><topic>Bacteria - drug effects</topic><topic>Bacteria - genetics</topic><topic>Bacteria - isolation & purification</topic><topic>Bioactive compounds</topic><topic>Catechin - analogs & derivatives</topic><topic>Catechin - pharmacology</topic><topic>Digestive system</topic><topic>Disease Models, Animal</topic><topic>Epigallocatechin gallate</topic><topic>Epithelium</topic><topic>Gastrointestinal Microbiome - drug effects</topic><topic>Gastrointestinal tract</topic><topic>Gene expression</topic><topic>Genes</topic><topic>Glucose Transport Proteins, Facilitative</topic><topic>Hyperuricemia</topic><topic>Hyperuricemia - drug therapy</topic><topic>Intestinal microflora</topic><topic>Intestine</topic><topic>Intestines - drug effects</topic><topic>Intestines - microbiology</topic><topic>Kidney - drug effects</topic><topic>Kidney - metabolism</topic><topic>Male</topic><topic>Metabolites</topic><topic>Metabolomics</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Microbiota</topic><topic>Microorganisms</topic><topic>Organic Anion Transporters - genetics</topic><topic>Organic Anion Transporters - metabolism</topic><topic>Oxonic Acid</topic><topic>Reabsorption</topic><topic>Relative abundance</topic><topic>rRNA 16S</topic><topic>Transcriptomics</topic><topic>Uric acid</topic><topic>Uric Acid - blood</topic><topic>Uric Acid - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Yu, Haonan</creatorcontrib><creatorcontrib>Lou, Zhenyou</creatorcontrib><creatorcontrib>Wu, Tingbo</creatorcontrib><creatorcontrib>Wan, Xiaochun</creatorcontrib><creatorcontrib>Huang, Haitao</creatorcontrib><creatorcontrib>Wu, Yuanyuan</creatorcontrib><creatorcontrib>Li, Bo</creatorcontrib><creatorcontrib>Tu, Youying</creatorcontrib><creatorcontrib>He, Puming</creatorcontrib><creatorcontrib>Liu, Junsheng</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Immunology Abstracts</collection><collection>Industrial and Applied Microbiology Abstracts (Microbiology A)</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Food & function</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Yu, Haonan</au><au>Lou, Zhenyou</au><au>Wu, Tingbo</au><au>Wan, Xiaochun</au><au>Huang, Haitao</au><au>Wu, Yuanyuan</au><au>Li, Bo</au><au>Tu, Youying</au><au>He, Puming</au><au>Liu, Junsheng</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Mechanisms of epigallocatechin gallate (EGCG) in ameliorating hyperuricemia: insights into gut microbiota and intestinal function in a mouse model</atitle><jtitle>Food & function</jtitle><addtitle>Food Funct</addtitle><date>2024-06-04</date><risdate>2024</risdate><volume>15</volume><issue>11</issue><spage>668</spage><epage>681</epage><pages>668-681</pages><issn>2042-6496</issn><eissn>2042-650X</eissn><abstract>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.</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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