Gut Microbiota-Derived Components and Metabolites in the Progression of Non-Alcoholic Fatty Liver Disease (NAFLD)
Human gut microbiota has been increasingly recognized as a pivotal determinant of non-alcoholic fatty liver disease (NAFLD). Apart from the changes in the composition of gut microbiota, the components and metabolites derived from intestinal microbiota have emerged as key factors in modulating the pa...
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Published in | Nutrients Vol. 11; no. 8; p. 1712 |
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Main Authors | , , , |
Format | Journal Article |
Language | English |
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25.07.2019
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Abstract | Human gut microbiota has been increasingly recognized as a pivotal determinant of non-alcoholic fatty liver disease (NAFLD). Apart from the changes in the composition of gut microbiota, the components and metabolites derived from intestinal microbiota have emerged as key factors in modulating the pathological process of NAFLD. Compelling evidences have revealed that gut microbiota generates a variety of bioactive substances that interact with the host liver cells through the portal vein. These substances include the components derived from bacteria such as lipopolysaccharides, peptidoglycan, DNA, and extracellular vesicles, as well as the metabolites ranging from short-chain fatty acids, indole and its derivatives, trimethylamine, secondary bile acids, to carotenoids and phenolic compounds. The mechanisms underlying the hepatic responses to the bioactive substances from gut bacteria have been associated with the regulation of glycolipid metabolism, immune signaling response, and redox homeostasis. Illuminating the interplay between the unique factors produced from gut microbiome and the liver will provide a novel therapeutical target for NAFLD. The current review highlights the recent advances on the mechanisms by which the key ingredients and metabolites from gut microbiota modulate the development and progression of NAFLD. |
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AbstractList | Human gut microbiota has been increasingly recognized as a pivotal determinant of non-alcoholic fatty liver disease (NAFLD). Apart from the changes in the composition of gut microbiota, the components and metabolites derived from intestinal microbiota have emerged as key factors in modulating the pathological process of NAFLD. Compelling evidences have revealed that gut microbiota generates a variety of bioactive substances that interact with the host liver cells through the portal vein. These substances include the components derived from bacteria such as lipopolysaccharides, peptidoglycan, DNA, and extracellular vesicles, as well as the metabolites ranging from short-chain fatty acids, indole and its derivatives, trimethylamine, secondary bile acids, to carotenoids and phenolic compounds. The mechanisms underlying the hepatic responses to the bioactive substances from gut bacteria have been associated with the regulation of glycolipid metabolism, immune signaling response, and redox homeostasis. Illuminating the interplay between the unique factors produced from gut microbiome and the liver will provide a novel therapeutical target for NAFLD. The current review highlights the recent advances on the mechanisms by which the key ingredients and metabolites from gut microbiota modulate the development and progression of NAFLD. Human gut microbiota has been increasingly recognized as a pivotal determinant of non-alcoholic fatty liver disease (NAFLD). Apart from the changes in the composition of gut microbiota, the components and metabolites derived from intestinal microbiota have emerged as key factors in modulating the pathological process of NAFLD. Compelling evidences have revealed that gut microbiota generates a variety of bioactive substances that interact with the host liver cells through the portal vein. These substances include the components derived from bacteria such as lipopolysaccharides, peptidoglycan, DNA, and extracellular vesicles, as well as the metabolites ranging from short-chain fatty acids, indole and its derivatives, trimethylamine, secondary bile acids, to carotenoids and phenolic compounds. The mechanisms underlying the hepatic responses to the bioactive substances from gut bacteria have been associated with the regulation of glycolipid metabolism, immune signaling response, and redox homeostasis. Illuminating the interplay between the unique factors produced from gut microbiome and the liver will provide a novel therapeutical target for NAFLD. The current review highlights the recent advances on the mechanisms by which the key ingredients and metabolites from gut microbiota modulate the development and progression of NAFLD.Human gut microbiota has been increasingly recognized as a pivotal determinant of non-alcoholic fatty liver disease (NAFLD). Apart from the changes in the composition of gut microbiota, the components and metabolites derived from intestinal microbiota have emerged as key factors in modulating the pathological process of NAFLD. Compelling evidences have revealed that gut microbiota generates a variety of bioactive substances that interact with the host liver cells through the portal vein. These substances include the components derived from bacteria such as lipopolysaccharides, peptidoglycan, DNA, and extracellular vesicles, as well as the metabolites ranging from short-chain fatty acids, indole and its derivatives, trimethylamine, secondary bile acids, to carotenoids and phenolic compounds. The mechanisms underlying the hepatic responses to the bioactive substances from gut bacteria have been associated with the regulation of glycolipid metabolism, immune signaling response, and redox homeostasis. Illuminating the interplay between the unique factors produced from gut microbiome and the liver will provide a novel therapeutical target for NAFLD. The current review highlights the recent advances on the mechanisms by which the key ingredients and metabolites from gut microbiota modulate the development and progression of NAFLD. |
Author | Yin, Yue Li, Ziru Ji, Yun Zhang, Weizhen |
AuthorAffiliation | 2 Department of Surgery, University of Michigan Medical Center, Ann Arbor, MI 48109-0346, USA 1 Department of Physiology and Pathophysiology, Peking University Health Science Center, Beijing 100191, China |
AuthorAffiliation_xml | – name: 1 Department of Physiology and Pathophysiology, Peking University Health Science Center, Beijing 100191, China – name: 2 Department of Surgery, University of Michigan Medical Center, Ann Arbor, MI 48109-0346, USA |
Author_xml | – sequence: 1 givenname: Yun orcidid: 0000-0002-3483-0729 surname: Ji fullname: Ji, Yun – sequence: 2 givenname: Yue surname: Yin fullname: Yin, Yue – sequence: 3 givenname: Ziru surname: Li fullname: Li, Ziru – sequence: 4 givenname: Weizhen orcidid: 0000-0001-8791-2798 surname: Zhang fullname: Zhang, Weizhen |
BackLink | https://www.ncbi.nlm.nih.gov/pubmed/31349604$$D View this record in MEDLINE/PubMed |
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