Role of Microbiota-Derived Metabolites in Alcoholic and Non-Alcoholic Fatty Liver Diseases
Chronic liver disease encompasses diseases that have various causes, such as alcoholic liver disease (ALD) and non-alcoholic fatty liver disease (NAFLD). Gut microbiota dysregulation plays a key role in the pathogenesis of ALD and NAFLD through the gut-liver axis. The gut microbiota consists of vari...
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| Veröffentlicht in: | International journal of molecular sciences 2021-12, Vol.23 (1), p.426 |
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| creator | Park, Ji-Won Kim, Sung-Eun Lee, Na Young Kim, Jung-Hee Jung, Jang-Han Jang, Myoung-Kuk Park, Sang-Hoon Lee, Myung-Seok Kim, Dong-Joon Kim, Hyoung-Su Suk, Ki Tae |
| description | Chronic liver disease encompasses diseases that have various causes, such as alcoholic liver disease (ALD) and non-alcoholic fatty liver disease (NAFLD). Gut microbiota dysregulation plays a key role in the pathogenesis of ALD and NAFLD through the gut-liver axis. The gut microbiota consists of various microorganisms that play a role in maintaining the homeostasis of the host and release a wide number of metabolites, including short-chain fatty acids (SCFAs), peptides, and hormones, continually shaping the host's immunity and metabolism. The integrity of the intestinal mucosal and vascular barriers is crucial to protect liver cells from exposure to harmful metabolites and pathogen-associated molecular pattern molecules. Dysbiosis and increased intestinal permeability may allow the liver to be exposed to abundant harmful metabolites that promote liver inflammation and fibrosis. In this review, we introduce the metabolites and components derived from the gut microbiota and discuss their pathologic effect in the liver alongside recent advances in molecular-based therapeutics and novel mechanistic findings associated with the gut-liver axis in ALD and NAFLD. |
| doi_str_mv | 10.3390/ijms23010426 |
| format | Article |
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Gut microbiota dysregulation plays a key role in the pathogenesis of ALD and NAFLD through the gut-liver axis. The gut microbiota consists of various microorganisms that play a role in maintaining the homeostasis of the host and release a wide number of metabolites, including short-chain fatty acids (SCFAs), peptides, and hormones, continually shaping the host's immunity and metabolism. The integrity of the intestinal mucosal and vascular barriers is crucial to protect liver cells from exposure to harmful metabolites and pathogen-associated molecular pattern molecules. Dysbiosis and increased intestinal permeability may allow the liver to be exposed to abundant harmful metabolites that promote liver inflammation and fibrosis. In this review, we introduce the metabolites and components derived from the gut microbiota and discuss their pathologic effect in the liver alongside recent advances in molecular-based therapeutics and novel mechanistic findings associated with the gut-liver axis in ALD and NAFLD.</description><identifier>ISSN: 1422-0067</identifier><identifier>ISSN: 1661-6596</identifier><identifier>EISSN: 1422-0067</identifier><identifier>DOI: 10.3390/ijms23010426</identifier><identifier>PMID: 35008852</identifier><language>eng</language><publisher>Switzerland: MDPI AG</publisher><subject>Alcohol ; Animals ; Autoimmune diseases ; Bacteria ; Bile ; Digestive system ; Dysbacteriosis ; Dysbiosis - microbiology ; Dysbiosis - therapy ; Ethanol ; Fatty acids ; Fatty liver ; Fibrosis ; Gastrointestinal Microbiome ; Gene expression ; Genomes ; Hepatocytes ; Homeostasis ; Humans ; Intestinal microflora ; Intestine ; Liver ; Liver cirrhosis ; Liver diseases ; Liver Diseases, Alcoholic - metabolism ; Liver Diseases, Alcoholic - microbiology ; Liver Diseases, Alcoholic - therapy ; Metabolic disorders ; Metabolites ; Metabolome ; Microbiota ; Microorganisms ; Models, Biological ; Mucosa ; Non-alcoholic Fatty Liver Disease - metabolism ; Non-alcoholic Fatty Liver Disease - microbiology ; Non-alcoholic Fatty Liver Disease - therapy ; Nutrition ; Pathogens ; Peptides ; Permeability ; Review ; Salmonella ; Signal transduction ; Tumor necrosis factor-TNF ; Veins & arteries</subject><ispartof>International journal of molecular sciences, 2021-12, Vol.23 (1), p.426</ispartof><rights>2021 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2021 by the authors. 2021</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c412t-d3c56b58c8bb9b4b118efd830a8747939fcf8532bc66d8e2ed3c9bbc910678473</citedby><cites>FETCH-LOGICAL-c412t-d3c56b58c8bb9b4b118efd830a8747939fcf8532bc66d8e2ed3c9bbc910678473</cites><orcidid>0000-0001-6236-780X ; 0000-0002-5884-9993 ; 0000-0002-7922-4634 ; 0000-0001-5435-6166</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC8745242/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC8745242/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,725,778,782,883,27911,27912,53778,53780</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/35008852$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Park, Ji-Won</creatorcontrib><creatorcontrib>Kim, Sung-Eun</creatorcontrib><creatorcontrib>Lee, Na Young</creatorcontrib><creatorcontrib>Kim, Jung-Hee</creatorcontrib><creatorcontrib>Jung, Jang-Han</creatorcontrib><creatorcontrib>Jang, Myoung-Kuk</creatorcontrib><creatorcontrib>Park, Sang-Hoon</creatorcontrib><creatorcontrib>Lee, Myung-Seok</creatorcontrib><creatorcontrib>Kim, Dong-Joon</creatorcontrib><creatorcontrib>Kim, Hyoung-Su</creatorcontrib><creatorcontrib>Suk, Ki Tae</creatorcontrib><title>Role of Microbiota-Derived Metabolites in Alcoholic and Non-Alcoholic Fatty Liver Diseases</title><title>International journal of molecular sciences</title><addtitle>Int J Mol Sci</addtitle><description>Chronic liver disease encompasses diseases that have various causes, such as alcoholic liver disease (ALD) and non-alcoholic fatty liver disease (NAFLD). Gut microbiota dysregulation plays a key role in the pathogenesis of ALD and NAFLD through the gut-liver axis. The gut microbiota consists of various microorganisms that play a role in maintaining the homeostasis of the host and release a wide number of metabolites, including short-chain fatty acids (SCFAs), peptides, and hormones, continually shaping the host's immunity and metabolism. The integrity of the intestinal mucosal and vascular barriers is crucial to protect liver cells from exposure to harmful metabolites and pathogen-associated molecular pattern molecules. Dysbiosis and increased intestinal permeability may allow the liver to be exposed to abundant harmful metabolites that promote liver inflammation and fibrosis. In this review, we introduce the metabolites and components derived from the gut microbiota and discuss their pathologic effect in the liver alongside recent advances in molecular-based therapeutics and novel mechanistic findings associated with the gut-liver axis in ALD and NAFLD.</description><subject>Alcohol</subject><subject>Animals</subject><subject>Autoimmune diseases</subject><subject>Bacteria</subject><subject>Bile</subject><subject>Digestive system</subject><subject>Dysbacteriosis</subject><subject>Dysbiosis - microbiology</subject><subject>Dysbiosis - therapy</subject><subject>Ethanol</subject><subject>Fatty acids</subject><subject>Fatty liver</subject><subject>Fibrosis</subject><subject>Gastrointestinal Microbiome</subject><subject>Gene expression</subject><subject>Genomes</subject><subject>Hepatocytes</subject><subject>Homeostasis</subject><subject>Humans</subject><subject>Intestinal microflora</subject><subject>Intestine</subject><subject>Liver</subject><subject>Liver cirrhosis</subject><subject>Liver diseases</subject><subject>Liver Diseases, Alcoholic - metabolism</subject><subject>Liver Diseases, Alcoholic - microbiology</subject><subject>Liver Diseases, Alcoholic - therapy</subject><subject>Metabolic disorders</subject><subject>Metabolites</subject><subject>Metabolome</subject><subject>Microbiota</subject><subject>Microorganisms</subject><subject>Models, Biological</subject><subject>Mucosa</subject><subject>Non-alcoholic Fatty Liver Disease - metabolism</subject><subject>Non-alcoholic Fatty Liver Disease - microbiology</subject><subject>Non-alcoholic Fatty Liver Disease - therapy</subject><subject>Nutrition</subject><subject>Pathogens</subject><subject>Peptides</subject><subject>Permeability</subject><subject>Review</subject><subject>Salmonella</subject><subject>Signal transduction</subject><subject>Tumor necrosis factor-TNF</subject><subject>Veins & arteries</subject><issn>1422-0067</issn><issn>1661-6596</issn><issn>1422-0067</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNpdkUtLAzEUhYMoVqs71xJw48LRPGamyUYovqEqiG7chCRzx6ZMJ5pMhf57Ux-1uspN7ncP9-QgtEfJMeeSnLjJNDJOKMlZuYa2aM5YRkg5WF-pe2g7xgkhjLNCbqIeLwgRomBb6PnBN4B9jW-dDd443-nsHIJ7hwrfQqeNb1wHEbsWDxvrx-lqsW4rfOfb7PflUnfdHI_SWMDnLoKOEHfQRq2bCLvfZx89XV48nl1no_urm7PhKLM5ZV1WcVuUphBWGCNNbigVUFeCEy0G-UByWdtaFJwZW5aVAAZpQBpjJU3GRD7gfXT6pfs6M1OoLLRd0I16DW6qw1x57dTfTuvG6sW_q6RfsJwlgcNvgeDfZhA7NXXRQtPoFvwsKlZSIUlZSpHQg3_oxM9Cm-x9UozLQiw2Ovqi0pfGGKBeLkOJWoSmVkNL-P6qgSX8kxL_ABC1ky0</recordid><startdate>20211231</startdate><enddate>20211231</enddate><creator>Park, Ji-Won</creator><creator>Kim, Sung-Eun</creator><creator>Lee, Na Young</creator><creator>Kim, Jung-Hee</creator><creator>Jung, Jang-Han</creator><creator>Jang, Myoung-Kuk</creator><creator>Park, Sang-Hoon</creator><creator>Lee, Myung-Seok</creator><creator>Kim, Dong-Joon</creator><creator>Kim, Hyoung-Su</creator><creator>Suk, Ki Tae</creator><general>MDPI AG</general><general>MDPI</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>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>MBDVC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>Q9U</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0001-6236-780X</orcidid><orcidid>https://orcid.org/0000-0002-5884-9993</orcidid><orcidid>https://orcid.org/0000-0002-7922-4634</orcidid><orcidid>https://orcid.org/0000-0001-5435-6166</orcidid></search><sort><creationdate>20211231</creationdate><title>Role of Microbiota-Derived Metabolites in Alcoholic and Non-Alcoholic Fatty Liver Diseases</title><author>Park, Ji-Won ; Kim, Sung-Eun ; Lee, Na Young ; Kim, Jung-Hee ; Jung, Jang-Han ; Jang, Myoung-Kuk ; Park, Sang-Hoon ; Lee, Myung-Seok ; Kim, Dong-Joon ; Kim, Hyoung-Su ; Suk, Ki Tae</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c412t-d3c56b58c8bb9b4b118efd830a8747939fcf8532bc66d8e2ed3c9bbc910678473</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>Alcohol</topic><topic>Animals</topic><topic>Autoimmune diseases</topic><topic>Bacteria</topic><topic>Bile</topic><topic>Digestive system</topic><topic>Dysbacteriosis</topic><topic>Dysbiosis - microbiology</topic><topic>Dysbiosis - therapy</topic><topic>Ethanol</topic><topic>Fatty acids</topic><topic>Fatty liver</topic><topic>Fibrosis</topic><topic>Gastrointestinal Microbiome</topic><topic>Gene expression</topic><topic>Genomes</topic><topic>Hepatocytes</topic><topic>Homeostasis</topic><topic>Humans</topic><topic>Intestinal microflora</topic><topic>Intestine</topic><topic>Liver</topic><topic>Liver cirrhosis</topic><topic>Liver diseases</topic><topic>Liver Diseases, Alcoholic - metabolism</topic><topic>Liver Diseases, Alcoholic - microbiology</topic><topic>Liver Diseases, Alcoholic - therapy</topic><topic>Metabolic disorders</topic><topic>Metabolites</topic><topic>Metabolome</topic><topic>Microbiota</topic><topic>Microorganisms</topic><topic>Models, Biological</topic><topic>Mucosa</topic><topic>Non-alcoholic Fatty Liver Disease - metabolism</topic><topic>Non-alcoholic Fatty Liver Disease - microbiology</topic><topic>Non-alcoholic Fatty Liver Disease - therapy</topic><topic>Nutrition</topic><topic>Pathogens</topic><topic>Peptides</topic><topic>Permeability</topic><topic>Review</topic><topic>Salmonella</topic><topic>Signal transduction</topic><topic>Tumor necrosis factor-TNF</topic><topic>Veins & arteries</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Park, Ji-Won</creatorcontrib><creatorcontrib>Kim, Sung-Eun</creatorcontrib><creatorcontrib>Lee, Na Young</creatorcontrib><creatorcontrib>Kim, Jung-Hee</creatorcontrib><creatorcontrib>Jung, Jang-Han</creatorcontrib><creatorcontrib>Jang, Myoung-Kuk</creatorcontrib><creatorcontrib>Park, Sang-Hoon</creatorcontrib><creatorcontrib>Lee, Myung-Seok</creatorcontrib><creatorcontrib>Kim, Dong-Joon</creatorcontrib><creatorcontrib>Kim, Hyoung-Su</creatorcontrib><creatorcontrib>Suk, Ki Tae</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Research Library (Alumni Edition)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>Research Library Prep</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Research Library</collection><collection>Research Library (Corporate)</collection><collection>Publicly Available Content Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central Basic</collection><collection>MEDLINE - 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Gut microbiota dysregulation plays a key role in the pathogenesis of ALD and NAFLD through the gut-liver axis. The gut microbiota consists of various microorganisms that play a role in maintaining the homeostasis of the host and release a wide number of metabolites, including short-chain fatty acids (SCFAs), peptides, and hormones, continually shaping the host's immunity and metabolism. The integrity of the intestinal mucosal and vascular barriers is crucial to protect liver cells from exposure to harmful metabolites and pathogen-associated molecular pattern molecules. Dysbiosis and increased intestinal permeability may allow the liver to be exposed to abundant harmful metabolites that promote liver inflammation and fibrosis. 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| source | MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; MDPI - Multidisciplinary Digital Publishing Institute; PubMed Central |
| subjects | Alcohol Animals Autoimmune diseases Bacteria Bile Digestive system Dysbacteriosis Dysbiosis - microbiology Dysbiosis - therapy Ethanol Fatty acids Fatty liver Fibrosis Gastrointestinal Microbiome Gene expression Genomes Hepatocytes Homeostasis Humans Intestinal microflora Intestine Liver Liver cirrhosis Liver diseases Liver Diseases, Alcoholic - metabolism Liver Diseases, Alcoholic - microbiology Liver Diseases, Alcoholic - therapy Metabolic disorders Metabolites Metabolome Microbiota Microorganisms Models, Biological Mucosa Non-alcoholic Fatty Liver Disease - metabolism Non-alcoholic Fatty Liver Disease - microbiology Non-alcoholic Fatty Liver Disease - therapy Nutrition Pathogens Peptides Permeability Review Salmonella Signal transduction Tumor necrosis factor-TNF Veins & arteries |
| title | Role of Microbiota-Derived Metabolites in Alcoholic and Non-Alcoholic Fatty Liver Diseases |
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