Molecular mechanisms of metabolic associated fatty liver disease (MAFLD): functional analysis of lipid metabolism pathways
The metabolic-associated fatty liver disease (MAFLD) is a condition of fat accumulation in the liver in combination with metabolic dysfunction in the form of overweight or obesity and insulin resistance. It is also associated with an increased cardiovascular disease risk, including hypertension and...
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| Published in | Clinical science (1979) Vol. 136; no. 18; pp. 1347 - 1366 |
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| Main Authors | , , , , |
| Format | Journal Article |
| Language | English |
| Published |
England
Portland Press Ltd
01.09.2022
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| Subjects | |
| Online Access | Get full text |
| ISSN | 0143-5221 1470-8736 1470-8736 |
| DOI | 10.1042/CS20220572 |
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| Abstract | The metabolic-associated fatty liver disease (MAFLD) is a condition of fat accumulation in the liver in combination with metabolic dysfunction in the form of overweight or obesity and insulin resistance. It is also associated with an increased cardiovascular disease risk, including hypertension and atherosclerosis. Hepatic lipid metabolism is regulated by a combination of the uptake and export of fatty acids, de novo lipogenesis, and fat utilization by β-oxidation. When the balance between these pathways is altered, hepatic lipid accumulation commences, and long-term activation of inflammatory and fibrotic pathways can progress to worsen the liver disease. This review discusses the details of the molecular mechanisms regulating hepatic lipids and the emerging therapies targeting these pathways as potential future treatments for MAFLD. |
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| AbstractList | The metabolic-associated fatty liver disease (MAFLD) is a condition of fat accumulation in the liver in combination with metabolic dysfunction in the form of overweight or obesity and insulin resistance. It is also associated with an increased cardiovascular disease risk, including hypertension and atherosclerosis. Hepatic lipid metabolism is regulated by a combination of the uptake and export of fatty acids, de novo lipogenesis, and fat utilization by β-oxidation. When the balance between these pathways is altered, hepatic lipid accumulation commences, and long-term activation of inflammatory and fibrotic pathways can progress to worsen the liver disease. This review discusses the details of the molecular mechanisms regulating hepatic lipids and the emerging therapies targeting these pathways as potential future treatments for MAFLD. The metabolic-associated fatty liver disease (MAFLD) is a condition of fat accumulation in the liver in combination with metabolic dysfunction in the form of overweight or obesity and insulin resistance. It is also associated with an increased cardiovascular disease risk, including hypertension and atherosclerosis. Hepatic lipid metabolism is regulated by a combination of the uptake and export of fatty acids, de novo lipogenesis, and fat utilization by β-oxidation. When the balance between these pathways is altered, hepatic lipid accumulation commences, and long-term activation of inflammatory and fibrotic pathways can progress to worsen the liver disease. This review discusses the details of the molecular mechanisms regulating hepatic lipids and the emerging therapies targeting these pathways as potential future treatments for MAFLD.The metabolic-associated fatty liver disease (MAFLD) is a condition of fat accumulation in the liver in combination with metabolic dysfunction in the form of overweight or obesity and insulin resistance. It is also associated with an increased cardiovascular disease risk, including hypertension and atherosclerosis. Hepatic lipid metabolism is regulated by a combination of the uptake and export of fatty acids, de novo lipogenesis, and fat utilization by β-oxidation. When the balance between these pathways is altered, hepatic lipid accumulation commences, and long-term activation of inflammatory and fibrotic pathways can progress to worsen the liver disease. This review discusses the details of the molecular mechanisms regulating hepatic lipids and the emerging therapies targeting these pathways as potential future treatments for MAFLD. |
| Author | Anderson, Christopher D. Badmus, Olufunto O. Stec, David E. Hinds, Terry D. Hillhouse, Sarah A. |
| AuthorAffiliation | 1 Department of Physiology and Biophysics, Cardiorenal, and Metabolic Diseases Research Center, University of Mississippi Medical Center, Jackson, MS 39216, U.S.A 3 Department of Pharmacology and Nutritional Sciences, Barnstable Brown Diabetes Center, Markey Cancer Center, University of Kentucky, Lexington, KY 40508, U.S.A 2 Department of Surgery, University of Mississippi Medical Center, Jackson, MS 39216, U.S.A |
| AuthorAffiliation_xml | – name: 2 Department of Surgery, University of Mississippi Medical Center, Jackson, MS 39216, U.S.A – name: 1 Department of Physiology and Biophysics, Cardiorenal, and Metabolic Diseases Research Center, University of Mississippi Medical Center, Jackson, MS 39216, U.S.A – name: 3 Department of Pharmacology and Nutritional Sciences, Barnstable Brown Diabetes Center, Markey Cancer Center, University of Kentucky, Lexington, KY 40508, U.S.A |
| Author_xml | – sequence: 1 givenname: Olufunto O. surname: Badmus fullname: Badmus, Olufunto O. – sequence: 2 givenname: Sarah A. surname: Hillhouse fullname: Hillhouse, Sarah A. – sequence: 3 givenname: Christopher D. surname: Anderson fullname: Anderson, Christopher D. – sequence: 4 givenname: Terry D. surname: Hinds fullname: Hinds, Terry D. – sequence: 5 givenname: David E. orcidid: 0000-0001-8359-4008 surname: Stec fullname: Stec, David E. |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/36148775$$D View this record in MEDLINE/PubMed |
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| PublicationYear | 2022 |
| Publisher | Portland Press Ltd |
| Publisher_xml | – name: Portland Press Ltd |
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