Molecular mechanisms of hepatic lipid accumulation in non-alcoholic fatty liver disease

Non-alcoholic fatty liver disease (NAFLD) is currently the world’s most common liver disease, estimated to affect up to one-fourth of the population. Hallmarked by hepatic steatosis, NAFLD is associated with a multitude of detrimental effects and increased mortality. This narrative review investigat...

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Published in	Cellular and molecular life sciences : CMLS Vol. 75; no. 18; pp. 3313 - 3327
Main Authors	Ipsen, David Højland, Lykkesfeldt, Jens, Tveden-Nyborg, Pernille
Format	Journal Article
Language	English
Published	Cham Springer International Publishing 01.09.2018 Springer Nature B.V
Subjects	Accumulation Animals Apoptosis beta oxidation biochemical pathways Biochemistry Biomedical and Life Sciences Biomedicine Cell Biology Cytochromes disease course Exports Fatty Acid Transport Proteins - metabolism Fatty acids Fatty Acids - metabolism Fatty liver Homeostasis Humans Hypoglycemic Agents - therapeutic use Life Sciences Lipid metabolism Lipid Metabolism - physiology Lipids Lipogenesis Liver Liver - metabolism Liver diseases Metabolism Mitochondria Mitochondria - metabolism Molecular chains Molecular modelling mortality Non-alcoholic Fatty Liver Disease - drug therapy Non-alcoholic Fatty Liver Disease - metabolism Non-alcoholic Fatty Liver Disease - pathology Normalizing Organs Oxidation Oxidative stress Peroxisomes Plateaus Reactive Oxygen Species - metabolism Review Steatosis uptake mechanisms Pharmacotherapy Animal models Lipid metabolism
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Abstract	Non-alcoholic fatty liver disease (NAFLD) is currently the world’s most common liver disease, estimated to affect up to one-fourth of the population. Hallmarked by hepatic steatosis, NAFLD is associated with a multitude of detrimental effects and increased mortality. This narrative review investigates the molecular mechanisms of hepatic steatosis in NAFLD, focusing on the four major pathways contributing to lipid homeostasis in the liver. Hepatic steatosis is a consequence of lipid acquisition exceeding lipid disposal, i.e., the uptake of fatty acids and de novo lipogenesis surpassing fatty acid oxidation and export. In NAFLD, hepatic uptake and de novo lipogenesis are increased, while a compensatory enhancement of fatty acid oxidation is insufficient in normalizing lipid levels and may even promote cellular damage and disease progression by inducing oxidative stress, especially with compromised mitochondrial function and increased oxidation in peroxisomes and cytochromes. While lipid export initially increases, it plateaus and may even decrease with disease progression, sustaining the accumulation of lipids. Fueled by lipo-apoptosis, hepatic steatosis leads to systemic metabolic disarray that adversely affects multiple organs, placing abnormal lipid metabolism associated with NAFLD in close relation to many of the current life-style-related diseases.
AbstractList	Non-alcoholic fatty liver disease (NAFLD) is currently the world’s most common liver disease, estimated to affect up to one-fourth of the population. Hallmarked by hepatic steatosis, NAFLD is associated with a multitude of detrimental effects and increased mortality. This narrative review investigates the molecular mechanisms of hepatic steatosis in NAFLD, focusing on the four major pathways contributing to lipid homeostasis in the liver. Hepatic steatosis is a consequence of lipid acquisition exceeding lipid disposal, i.e., the uptake of fatty acids and de novo lipogenesis surpassing fatty acid oxidation and export. In NAFLD, hepatic uptake and de novo lipogenesis are increased, while a compensatory enhancement of fatty acid oxidation is insufficient in normalizing lipid levels and may even promote cellular damage and disease progression by inducing oxidative stress, especially with compromised mitochondrial function and increased oxidation in peroxisomes and cytochromes. While lipid export initially increases, it plateaus and may even decrease with disease progression, sustaining the accumulation of lipids. Fueled by lipo-apoptosis, hepatic steatosis leads to systemic metabolic disarray that adversely affects multiple organs, placing abnormal lipid metabolism associated with NAFLD in close relation to many of the current life-style-related diseases. Non-alcoholic fatty liver disease (NAFLD) is currently the world's most common liver disease, estimated to affect up to one-fourth of the population. Hallmarked by hepatic steatosis, NAFLD is associated with a multitude of detrimental effects and increased mortality. This narrative review investigates the molecular mechanisms of hepatic steatosis in NAFLD, focusing on the four major pathways contributing to lipid homeostasis in the liver. Hepatic steatosis is a consequence of lipid acquisition exceeding lipid disposal, i.e., the uptake of fatty acids and de novo lipogenesis surpassing fatty acid oxidation and export. In NAFLD, hepatic uptake and de novo lipogenesis are increased, while a compensatory enhancement of fatty acid oxidation is insufficient in normalizing lipid levels and may even promote cellular damage and disease progression by inducing oxidative stress, especially with compromised mitochondrial function and increased oxidation in peroxisomes and cytochromes. While lipid export initially increases, it plateaus and may even decrease with disease progression, sustaining the accumulation of lipids. Fueled by lipo-apoptosis, hepatic steatosis leads to systemic metabolic disarray that adversely affects multiple organs, placing abnormal lipid metabolism associated with NAFLD in close relation to many of the current life-style-related diseases.Non-alcoholic fatty liver disease (NAFLD) is currently the world's most common liver disease, estimated to affect up to one-fourth of the population. Hallmarked by hepatic steatosis, NAFLD is associated with a multitude of detrimental effects and increased mortality. This narrative review investigates the molecular mechanisms of hepatic steatosis in NAFLD, focusing on the four major pathways contributing to lipid homeostasis in the liver. Hepatic steatosis is a consequence of lipid acquisition exceeding lipid disposal, i.e., the uptake of fatty acids and de novo lipogenesis surpassing fatty acid oxidation and export. In NAFLD, hepatic uptake and de novo lipogenesis are increased, while a compensatory enhancement of fatty acid oxidation is insufficient in normalizing lipid levels and may even promote cellular damage and disease progression by inducing oxidative stress, especially with compromised mitochondrial function and increased oxidation in peroxisomes and cytochromes. While lipid export initially increases, it plateaus and may even decrease with disease progression, sustaining the accumulation of lipids. Fueled by lipo-apoptosis, hepatic steatosis leads to systemic metabolic disarray that adversely affects multiple organs, placing abnormal lipid metabolism associated with NAFLD in close relation to many of the current life-style-related diseases.
Author	Lykkesfeldt, Jens Tveden-Nyborg, Pernille Ipsen, David Højland
Author_xml	– sequence: 1 givenname: David Højland surname: Ipsen fullname: Ipsen, David Højland organization: Department of Veterinary and Animal Sciences, Faculty of Health and Medical Sciences, University of Copenhagen – sequence: 2 givenname: Jens surname: Lykkesfeldt fullname: Lykkesfeldt, Jens organization: Department of Veterinary and Animal Sciences, Faculty of Health and Medical Sciences, University of Copenhagen – sequence: 3 givenname: Pernille surname: Tveden-Nyborg fullname: Tveden-Nyborg, Pernille email: ptn@sund.ku.dk organization: Department of Veterinary and Animal Sciences, Faculty of Health and Medical Sciences, University of Copenhagen
BackLink	https://www.ncbi.nlm.nih.gov/pubmed/29936596$$D View this record in MEDLINE/PubMed
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Issue	18
Keywords	Pharmacotherapy Animal models Lipid metabolism
Language	English
License	Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made.
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PublicationTitle	Cellular and molecular life sciences : CMLS
PublicationTitleAbbrev	Cell. Mol. Life Sci
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PublicationYear	2018
Publisher	Springer International Publishing Springer Nature B.V
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Snippet	Non-alcoholic fatty liver disease (NAFLD) is currently the world’s most common liver disease, estimated to affect up to one-fourth of the population.... Non-alcoholic fatty liver disease (NAFLD) is currently the world's most common liver disease, estimated to affect up to one-fourth of the population....
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SubjectTerms	Accumulation Animals Apoptosis beta oxidation biochemical pathways Biochemistry Biomedical and Life Sciences Biomedicine Cell Biology Cytochromes disease course Exports Fatty Acid Transport Proteins - metabolism Fatty acids Fatty Acids - metabolism Fatty liver Homeostasis Humans Hypoglycemic Agents - therapeutic use Life Sciences Lipid metabolism Lipid Metabolism - physiology Lipids Lipogenesis Liver Liver - metabolism Liver diseases Metabolism Mitochondria Mitochondria - metabolism Molecular chains Molecular modelling mortality Non-alcoholic Fatty Liver Disease - drug therapy Non-alcoholic Fatty Liver Disease - metabolism Non-alcoholic Fatty Liver Disease - pathology Normalizing Organs Oxidation Oxidative stress Peroxisomes Plateaus Reactive Oxygen Species - metabolism Review Steatosis uptake mechanisms
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Title	Molecular mechanisms of hepatic lipid accumulation in non-alcoholic fatty liver disease
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