Non-alcoholic fatty liver disease. From insulin resistance to mitochondrial dysfunction
Non-alcoholic fatty liver disease represents a set of liver lesions similar to those induced by alcohol that develop in individuals with no alcohol abuse. When lesions consist of fatty and hydropic degeneration, inflammation, and eventually fibrosis, the condition is designated non-alcoholic steatoh...
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| Published in: | Revista española de enfermedades digestivas Vol. 98; no. 11; pp. 844 - 874 |
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| Abstract | Non-alcoholic fatty liver disease represents a set of liver lesions similar to those induced by alcohol that develop in individuals with no alcohol abuse. When lesions consist of fatty and hydropic degeneration, inflammation, and eventually fibrosis, the condition is designated non-alcoholic steatohepatitis (NASH). The pathogenesis of these lesions is not clearly understood, but they are associated with insulin resistance in most cases. As a result, abdominal fat tissue lipolysis and excessive fatty acid uptake by the liver occur. This, together with a disturbance of triglyceride export as VLDL, results in fatty liver development. Both the inflammatory and hepatocellular degenerative components of NASH are attributed to oxidative stress. Mitochondrial respiratory chain loss of activity plays a critical role in the genesis of latter stress. This may be initiated by an increase in the hepatic TNFalpha, iNOS induction, peroxynitrite formation, tyrosine nitration and inactivation of enzymes making up this chain. Consequences of oxidative stress include: lipid peroxidation in cell membranes, stellate cell activation in the liver, liver fibrosis, chronic inflammation, and apoptosis. |
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| AbstractList | Non-alcoholic fatty liver disease represents a set of liver lesions similar to those induced by alcohol that develop in individuals with no alcohol abuse. When lesions consist of fatty and hydropic degeneration, inflammation, and eventually fibrosis, the condition is designated non-alcoholic steatohepatitis (NASH). The pathogenesis of these lesions is not clearly understood, but they are associated with insulin resistance in most cases. As a result, abdominal fat tissue lipolysis and excessive fatty acid uptake by the liver occur. This, together with a disturbance of triglyceride export as VLDL, results in fatty liver development. Both the inflammatory and hepatocellular degenerative components of NASH are attributed to oxidative stress. Mitochondrial respiratory chain loss of activity plays a critical role in the genesis of latter stress. This may be initiated by an increase in the hepatic TNFa, iNOS induction, peroxynitrite formation, tyrosine nitration and inactivation of enzymes making up this chain. Consequences of oxidative stress include: lipid peroxidation in cell membranes, stellate cell activation in the liver, liver fibrosis, chronic inflammation, and apoptosis. Non-alcoholic fatty liver disease represents a set of liver lesions similar to those induced by alcohol that develop in individuals with no alcohol abuse. When lesions consist of fatty and hydropic degeneration, inflammation, and eventually fibrosis, the condition is designated non-alcoholic steatohepatitis (NASH). The pathogenesis of these lesions is not clearly understood, but they are associated with insulin resistance in most cases. As a result, abdominal fat tissue lipolysis and excessive fatty acid uptake by the liver occur. This, together with a disturbance of triglyceride export as VLDL, results in fatty liver development. Both the inflammatory and hepatocellular degenerative components of NASH are attributed to oxidative stress. Mitochondrial respiratory chain loss of activity plays a critical role in the genesis of latter stress. This may be initiated by an increase in the hepatic TNFalpha, iNOS induction, peroxynitrite formation, tyrosine nitration and inactivation of enzymes making up this chain. Consequences of oxidative stress include: lipid peroxidation in cell membranes, stellate cell activation in the liver, liver fibrosis, chronic inflammation, and apoptosis. |
| Author | Pérez Carreras, M Muñoz Yagüe, M T Solís Herruzo, J A García Ruiz, I |
| AuthorAffiliation | Universidad Complutense de Madrid |
| AuthorAffiliation_xml | – name: Universidad Complutense de Madrid |
| Author_xml | – sequence: 1 givenname: J A surname: Solís Herruzo fullname: Solís Herruzo, J A email: jsolis.hdoc@salud.madrid.org organization: Department of Gastroenterology, University Hospital 12 de Octubre, Madrid, Spain. jsolis.hdoc@salud.madrid.org – sequence: 2 givenname: I surname: García Ruiz fullname: García Ruiz, I – sequence: 3 givenname: M surname: Pérez Carreras fullname: Pérez Carreras, M – sequence: 4 givenname: M T surname: Muñoz Yagüe fullname: Muñoz Yagüe, M T |
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| CitedBy_id | crossref_primary_10_1111_liv_12741 crossref_primary_10_1194_jlr_M800418_JLR200 crossref_primary_10_2169_internalmedicine_9490_17 crossref_primary_10_1097_MPA_0b013e3181a9d5af crossref_primary_10_1038_oby_2009_58 crossref_primary_10_1016_j_bbrc_2017_06_047 crossref_primary_10_1002_hep_22039 crossref_primary_10_1186_1476_511X_10_122 crossref_primary_10_17235_reed_2017_4981_2017 crossref_primary_10_3748_wjg_15_1929 crossref_primary_10_1016_j_arteri_2015_03_003 crossref_primary_10_1016_j_bbabio_2007_07_011 crossref_primary_10_4236_ojgas_2014_45030 |
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| Keywords | Non-alcoholic fatty liver disease Insulin resistance Mitochondrial dysfunction |
| Language | English |
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| Snippet | Non-alcoholic fatty liver disease represents a set of liver lesions similar to those induced by alcohol that develop in individuals with no alcohol abuse. When... |
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| SubjectTerms | Clinical Trials as Topic Fatty Liver - metabolism Gastroenterology & Hepatology Geriatrics & Gerontology Humans Infectious Diseases Insulin Resistance - physiology Mitochondria, Liver - metabolism Oncology Oxidative Stress - physiology Pathology Pharmacology & Pharmacy Radiology, Nuclear Medicine & Medical Imaging Surgery |
| Title | Non-alcoholic fatty liver disease. From insulin resistance to mitochondrial dysfunction |
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