Interactions between gut microbiota and non-alcoholic liver disease: The role of microbiota-derived metabolites

[Display omitted] There is increasing evidence that the intestinal microbiota plays a mechanistic role in the etiology of non-alcoholic fatty liver disease (NAFLD). Animal and human studies have linked small molecule metabolites produced by commensal bacteria in the gut contribute to not only intest...

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Published in	Pharmacological research Vol. 141; pp. 521 - 529
Main Authors	Ding, Yufang, Yanagi, Karin, Cheng, Clint, Alaniz, Robert C., Lee, Kyongbum, Jayaraman, Arul
Format	Journal Article
Language	English
Published	Netherlands Elsevier Ltd 01.03.2019
Subjects	Amino Acids - immunology Amino Acids - metabolism Animals Bacteria - immunology Bacteria - metabolism Bile acids Bile Acids and Salts - immunology Bile Acids and Salts - metabolism Dysbiosis - complications Dysbiosis - immunology Dysbiosis - metabolism Fatty Acids, Volatile - immunology Fatty Acids, Volatile - metabolism Gastrointestinal Microbiome Humans Indole Inflammation Inflammation - etiology Inflammation - immunology Inflammation - metabolism Microbiota metabolites NAFLD Non-alcoholic Fatty Liver Disease - etiology Non-alcoholic Fatty Liver Disease - immunology Non-alcoholic Fatty Liver Disease - metabolism Short chain fatty acids FXR NAFLD Microbiota metabolites Tributyrin (PubMed CID: 6050) TUDCA Indole HFD UDCA Indole (PubMed CID: 798) Short chain fatty acids LPS Taurine (PubMed CID: 1123) Butyrate (PubMed CID: 104775) Indole-3-acetic acid (PubMed CID: 802) Cholic acid (PubMed CID: 221493) Tryptophan (PubMed CID: 6305) Propionate (PubMed CID: 104745) DCA GLP-1 Bile acids Acetate (PubMed CID: 175) MCA Inflammation NASH Tryptamine (PubMed CID: 1150) SCFAs
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Abstract	[Display omitted] There is increasing evidence that the intestinal microbiota plays a mechanistic role in the etiology of non-alcoholic fatty liver disease (NAFLD). Animal and human studies have linked small molecule metabolites produced by commensal bacteria in the gut contribute to not only intestinal inflammation, but also to hepatic inflammation. These immunomodulatory metabolites are capable of engaging host cellular receptors, and may mediate the observed association between gut dysbiosis and NAFLD. This review focuses on the effects and potential mechanisms of three specific classes of metabolites that synthesized or modified by gut bacteria: short chain fatty acids, amino acid catabolites, and bile acids. In particular, we discuss their role as ligands for cell surface and nuclear receptors regulating metabolic and inflammatory pathways in the intestine and liver. Studies reveal that the metabolites can both agonize and antagonize their cognate receptors to reduce or exacerbate liver steatosis and inflammation, and that the effects are metabolite- and context-specific. Further studies are warranted to more comprehensively understand bacterial metabolite-mediated gut-liver in NAFLD. This understanding could help identify novel therapeutics and therapeutic targets to intervene in the disease through the gut microbiota.
AbstractList	[Display omitted] There is increasing evidence that the intestinal microbiota plays a mechanistic role in the etiology of non-alcoholic fatty liver disease (NAFLD). Animal and human studies have linked small molecule metabolites produced by commensal bacteria in the gut contribute to not only intestinal inflammation, but also to hepatic inflammation. These immunomodulatory metabolites are capable of engaging host cellular receptors, and may mediate the observed association between gut dysbiosis and NAFLD. This review focuses on the effects and potential mechanisms of three specific classes of metabolites that synthesized or modified by gut bacteria: short chain fatty acids, amino acid catabolites, and bile acids. In particular, we discuss their role as ligands for cell surface and nuclear receptors regulating metabolic and inflammatory pathways in the intestine and liver. Studies reveal that the metabolites can both agonize and antagonize their cognate receptors to reduce or exacerbate liver steatosis and inflammation, and that the effects are metabolite- and context-specific. Further studies are warranted to more comprehensively understand bacterial metabolite-mediated gut-liver in NAFLD. This understanding could help identify novel therapeutics and therapeutic targets to intervene in the disease through the gut microbiota. There is increasing evidence that the intestinal microbiota plays a mechanistic role in the etiology of non-alcoholic fatty liver disease (NAFLD). Animal and human studies have linked small molecule metabolites produced by commensal bacteria in the gut contribute to not only intestinal inflammation, but also to hepatic inflammation. These immunomodulatory metabolites are capable of engaging host cellular receptors, and may mediate the observed association between gut dysbiosis and NAFLD. This review focuses on the effects and potential mechanisms of three specific classes of metabolites that synthesized or modified by gut bacteria: short chain fatty acids, amino acid catabolites, and bile acids. In particular, we discuss their role as ligands for cell surface and nuclear receptors regulating metabolic and inflammatory pathways in the intestine and liver. Studies reveal that the metabolites can both agonize and antagonize their cognate receptors to reduce or exacerbate liver steatosis and inflammation, and that the effects are metabolite- and context-specific. Further studies are warranted to more comprehensively understand bacterial metabolite-mediated gut-liver in NAFLD. This understanding could help identify novel therapeutics and therapeutic targets to intervene in the disease through the gut microbiota.There is increasing evidence that the intestinal microbiota plays a mechanistic role in the etiology of non-alcoholic fatty liver disease (NAFLD). Animal and human studies have linked small molecule metabolites produced by commensal bacteria in the gut contribute to not only intestinal inflammation, but also to hepatic inflammation. These immunomodulatory metabolites are capable of engaging host cellular receptors, and may mediate the observed association between gut dysbiosis and NAFLD. This review focuses on the effects and potential mechanisms of three specific classes of metabolites that synthesized or modified by gut bacteria: short chain fatty acids, amino acid catabolites, and bile acids. In particular, we discuss their role as ligands for cell surface and nuclear receptors regulating metabolic and inflammatory pathways in the intestine and liver. Studies reveal that the metabolites can both agonize and antagonize their cognate receptors to reduce or exacerbate liver steatosis and inflammation, and that the effects are metabolite- and context-specific. Further studies are warranted to more comprehensively understand bacterial metabolite-mediated gut-liver in NAFLD. This understanding could help identify novel therapeutics and therapeutic targets to intervene in the disease through the gut microbiota. There is increasing evidence that the intestinal microbiota plays a mechanistic role in the etiology of non-alcoholic fatty liver disease (NAFLD). Animal and human studies have linked small molecule metabolites produced by commensal bacteria in the gut contribute to not only intestinal inflammation, but also to hepatic inflammation. These immunomodulatory metabolites are capable of engaging host cellular receptors, and may mediate the observed association between gut dysbiosis and NAFLD. This review focuses on the effects and potential mechanisms of three specific classes of metabolites that synthesized or modified by gut bacteria: short chain fatty acids, amino acid catabolites, and bile acids. In particular, we discuss their role as ligands for cell surface and nuclear receptors regulating metabolic and inflammatory pathways in the intestine and liver. Studies reveal that the metabolites can both agonize and antagonize their cognate receptors to reduce or exacerbate liver steatosis and inflammation, and that the effects are metabolite- and context-specific. Further studies are warranted to more comprehensively understand bacterial metabolite-mediated gut-liver in NAFLD. This understanding could help identify novel therapeutics and therapeutic targets to intervene in the disease through the gut microbiota.
Author	Cheng, Clint Alaniz, Robert C. Jayaraman, Arul Yanagi, Karin Ding, Yufang Lee, Kyongbum
AuthorAffiliation	d Artie McFerrin Department of Chemical Engineering, Texas A&M University, College Station, Texas 77843, USA b Department of Chemical and Biological Engineering, Tufts University, Medford, MA 02155 c Department of Microbial Pathogenesis and Immunology, Texas A&M Health Science Center, Bryan, TX 77807 a Department of Biomedical Engineering, Texas A&M University, College Station, TX 77843
AuthorAffiliation_xml	– name: b Department of Chemical and Biological Engineering, Tufts University, Medford, MA 02155 – name: c Department of Microbial Pathogenesis and Immunology, Texas A&M Health Science Center, Bryan, TX 77807 – name: a Department of Biomedical Engineering, Texas A&M University, College Station, TX 77843 – name: d Artie McFerrin Department of Chemical Engineering, Texas A&M University, College Station, Texas 77843, USA
Author_xml	– sequence: 1 givenname: Yufang surname: Ding fullname: Ding, Yufang organization: Department of Biomedical Engineering, Texas A&M University, College Station, TX, 77843, USA – sequence: 2 givenname: Karin surname: Yanagi fullname: Yanagi, Karin organization: Department of Chemical and Biological Engineering, Tufts University, Medford, MA, 02155, USA – sequence: 3 givenname: Clint surname: Cheng fullname: Cheng, Clint organization: Department of Microbial Pathogenesis and Immunology, Texas A&M Health Science Center, Bryan, TX, 77807, USA – sequence: 4 givenname: Robert C. surname: Alaniz fullname: Alaniz, Robert C. organization: Department of Microbial Pathogenesis and Immunology, Texas A&M Health Science Center, Bryan, TX, 77807, USA – sequence: 5 givenname: Kyongbum surname: Lee fullname: Lee, Kyongbum email: kyongbum.lee@tufts.edu organization: Department of Chemical and Biological Engineering, Tufts University, Medford, MA, 02155, USA – sequence: 6 givenname: Arul surname: Jayaraman fullname: Jayaraman, Arul email: arulj@tamu.edu organization: Department of Biomedical Engineering, Texas A&M University, College Station, TX, 77843, USA
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Keywords	FXR NAFLD Microbiota metabolites Tributyrin (PubMed CID: 6050) TUDCA Indole HFD UDCA Indole (PubMed CID: 798) Short chain fatty acids LPS Taurine (PubMed CID: 1123) Butyrate (PubMed CID: 104775) Indole-3-acetic acid (PubMed CID: 802) Cholic acid (PubMed CID: 221493) Tryptophan (PubMed CID: 6305) Propionate (PubMed CID: 104745) DCA GLP-1 Bile acids Acetate (PubMed CID: 175) MCA Inflammation NASH Tryptamine (PubMed CID: 1150) SCFAs
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Snippet	[Display omitted] There is increasing evidence that the intestinal microbiota plays a mechanistic role in the etiology of non-alcoholic fatty liver disease... There is increasing evidence that the intestinal microbiota plays a mechanistic role in the etiology of non-alcoholic fatty liver disease (NAFLD). Animal and...
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SubjectTerms	Amino Acids - immunology Amino Acids - metabolism Animals Bacteria - immunology Bacteria - metabolism Bile acids Bile Acids and Salts - immunology Bile Acids and Salts - metabolism Dysbiosis - complications Dysbiosis - immunology Dysbiosis - metabolism Fatty Acids, Volatile - immunology Fatty Acids, Volatile - metabolism Gastrointestinal Microbiome Humans Indole Inflammation Inflammation - etiology Inflammation - immunology Inflammation - metabolism Microbiota metabolites NAFLD Non-alcoholic Fatty Liver Disease - etiology Non-alcoholic Fatty Liver Disease - immunology Non-alcoholic Fatty Liver Disease - metabolism Short chain fatty acids
Title	Interactions between gut microbiota and non-alcoholic liver disease: The role of microbiota-derived metabolites
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