Hypoxia and non-alcoholic fatty liver disease
NAFLD (non-alcoholic fatty liver disease) represents a spectrum of fatty liver diseases associated with an increased risk of Type 2 diabetes and cardiovascular disease. The spectrum of fatty liver diseases comprises simple steatosis, steatosis with inflammation [i.e. NASH (non-alcoholic steatohepati...
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| Published in | Clinical science (1979) Vol. 118; no. 6; pp. 397 - 400 |
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| Main Author | |
| Format | Journal Article |
| Language | English |
| Published |
England
Portland Press
14.12.2009
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| Subjects | |
| Online Access | Get full text |
| ISSN | 0143-5221 1470-8736 1470-8736 |
| DOI | 10.1042/CS20090565 |
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| Abstract | NAFLD (non-alcoholic fatty liver disease) represents a spectrum of fatty liver diseases associated with an increased risk of Type 2 diabetes and cardiovascular disease. The spectrum of fatty liver diseases comprises simple steatosis, steatosis with inflammation [i.e. NASH (non-alcoholic steatohepatitis)], fatty liver disease with inflammation and fibrosis (severe NASH) and cirrhosis. The molecular mechanisms contributing to NASH are the subject of considerable investigation, as a better understanding of the pathogenesis of NASH will lead to novel therapies for a condition that hitherto remains difficult to treat. In the present issue of Clinical Science, Piguet and co-workers have investigated the effects of hypoxia in the PTEN (phosphatase and tensin homologue deleted on chromosome 10)-deficient mouse, a mouse model that develops NAFLD. The authors show that a short period (7 days) of exposure to hypoxia aggravates the NAFLD phenotype, causing changes in the liver that are in keeping with NASH with increased lipogenesis and inflammation. |
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| AbstractList | NAFLD (non-alcoholic fatty liver disease) represents a spectrum of fatty liver diseases associated with an increased risk of Type 2 diabetes and cardiovascular disease. The spectrum of fatty liver diseases comprises simple steatosis, steatosis with inflammation [i.e. NASH (non-alcoholic steatohepatitis)], fatty liver disease with inflammation and fibrosis (severe NASH) and cirrhosis. The molecular mechanisms contributing to NASH are the subject of considerable investigation, as a better understanding of the pathogenesis of NASH will lead to novel therapies for a condition that hitherto remains difficult to treat. In the present issue of Clinical Science, Piguet and co-workers have investigated the effects of hypoxia in the PTEN (phosphatase and tensin homologue deleted on chromosome 10)-deficient mouse, a mouse model that develops NAFLD. The authors show that a short period (7 days) of exposure to hypoxia aggravates the NAFLD phenotype, causing changes in the liver that are in keeping with NASH with increased lipogenesis and inflammation.NAFLD (non-alcoholic fatty liver disease) represents a spectrum of fatty liver diseases associated with an increased risk of Type 2 diabetes and cardiovascular disease. The spectrum of fatty liver diseases comprises simple steatosis, steatosis with inflammation [i.e. NASH (non-alcoholic steatohepatitis)], fatty liver disease with inflammation and fibrosis (severe NASH) and cirrhosis. The molecular mechanisms contributing to NASH are the subject of considerable investigation, as a better understanding of the pathogenesis of NASH will lead to novel therapies for a condition that hitherto remains difficult to treat. In the present issue of Clinical Science, Piguet and co-workers have investigated the effects of hypoxia in the PTEN (phosphatase and tensin homologue deleted on chromosome 10)-deficient mouse, a mouse model that develops NAFLD. The authors show that a short period (7 days) of exposure to hypoxia aggravates the NAFLD phenotype, causing changes in the liver that are in keeping with NASH with increased lipogenesis and inflammation. NAFLD (non-alcoholic fatty liver disease) represents a spectrum of fatty liver diseases associated with an increased risk of Type 2 diabetes and cardiovascular disease. The spectrum of fatty liver diseases comprises simple steatosis, steatosis with inflammation [i.e. NASH (non-alcoholic steatohepatitis)], fatty liver disease with inflammation and fibrosis (severe NASH) and cirrhosis. The molecular mechanisms contributing to NASH are the subject of considerable investigation, as a better understanding of the pathogenesis of NASH will lead to novel therapies for a condition that hitherto remains difficult to treat. In the present issue of Clinical Science, Piguet and co-workers have investigated the effects of hypoxia in the PTEN (phosphatase and tensin homologue deleted on chromosome 10)-deficient mouse, a mouse model that develops NAFLD. The authors show that a short period (7 days) of exposure to hypoxia aggravates the NAFLD phenotype, causing changes in the liver that are in keeping with NASH with increased lipogenesis and inflammation. Non alcoholic fatty liver disease (NAFLD) represents a spectrum of fatty liver diseases associated with increased risk of type 2 diabetes and cardiovascular disease. The spectrum of fatty liver diseases, comprises simple steatosis, steatosis with inflammation (i.e. non alcoholic steatohepatitis or NASH), fatty liver disease with inflammation and fibrosis (severe NASH) and cirrhosis. The molecular mechanisms contributing to NASH are the subject of considerable investigation, as a better understanding of the pathogenesis of NASH will lead to novel therapies for a condition that hitherto remains difficult to treat. In this edition of the Journal Piquet et al have investigated the effects of hypoxia in the PTEN deficient mouse, a mouse model that develops NAFLD. Piquet et al show that a short period (7 days) of exposure to hypoxia aggravates the NAFLD phenotype, causing changes in the liver that are in keeping with NASH, with increased lipogenesis and inflammation. NAFLD (non-alcoholic fatty liver disease) represents a spectrum of fatty liver diseases associated with an increased risk of Type 2 diabetes and cardiovascular disease. The spectrum of fatty liver diseases comprises simple steatosis, steatosis with inflammation [i.e. NASH (non-alcoholic steatohepatitis)], fatty liver disease with inflammation and fibrosis (severe NASH) and cirrhosis. The molecular mechanisms contributing to NASH are the subject of considerable investigation, as a better understanding of the pathogenesis of NASH will lead to novel therapies for a condition that hitherto remains difficult to treat. In the present issue of Clinical Science, Piguet and co-workers have investigated the effects of hypoxia in the PTEN (phosphatase and tensin homologue deleted on chromosome 10)-deficient mouse, a mouse model that develops NAFLD. The authors show that a short period (7 days) of exposure to hypoxia aggravates the NAFLD phenotype, causing changes in the liver that are in keeping with NASH with increased lipogenesis and inflammation. |
| Author | Byrne, Christopher D. |
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| Cites_doi | 10.1128/MCB.24.3.1007-1021.2004 10.1042/CS20090313 10.1111/j.1440-1746.2006.04665.x 10.1210/mend.15.8.0684 10.1073/pnas.0308617100 10.1073/pnas.90.12.5723 10.1074/jbc.M210062200 10.1074/jbc.M106703200 10.1074/jbc.M501949200 10.1083/jcb.200403069 10.1172/JCI20513 10.1074/jbc.275.17.12889 10.1002/hep.23205 10.1080/13813450600711359 10.1053/j.gastro.2007.10.010 10.1055/s-2004-826016 10.1042/CS20080253 |
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| References_xml | – volume: 24 start-page: 1007 year: 2004 ident: 2021113010162211100_B16 article-title: Suppression of PTEN expression by NF-κB prevents apoptosis publication-title: Mol. Cell Biol. doi: 10.1128/MCB.24.3.1007-1021.2004 – volume: 118 start-page: 401 year: 2010 ident: 2021113010162211100_B2 article-title: Hypoxia aggravates non-alcoholic steatohepatitis in mice lacking hepatocellular PTEN publication-title: Clin. Sci. doi: 10.1042/CS20090313 – volume: 22 start-page: S96 year: 2007 ident: 2021113010162211100_B5 article-title: Non-alcoholic steatohepatitis and hepatocellular carcinoma: lessons from hepatocyte-specific phosphatase and tensin homolog (PTEN)-deficient mice publication-title: J. Gastroenterol. Hepatol. doi: 10.1111/j.1440-1746.2006.04665.x – volume: 15 start-page: 1411 year: 2001 ident: 2021113010162211100_B9 article-title: Regulation of phosphoinositide metabolism, Akt phosphorylation, and glucose transport by PTEN (phosphatase and tensin homolog deleted on chromosome 10) in 3T3-L1 adipocytes publication-title: Mol. Endocrinol. doi: 10.1210/mend.15.8.0684 – volume: 101 start-page: 2082 year: 2004 ident: 2021113010162211100_B13 article-title: Liver-specific deletion of negative regulator Pten results in fatty liver and insulin hypersensitivity publication-title: Proc. Natl. Acad. Sci. U.S.A. doi: 10.1073/pnas.0308617100 – volume: 90 start-page: 5723 year: 1993 ident: 2021113010162211100_B14 article-title: Diverse peroxisome proliferator-activated receptors bind to the peroxisome proliferator-responsive elements of the rat hydratase/dehydrogenase and fatty acyl-CoA oxidase genes but differentially induce expression publication-title: Proc. Natl. Acad. Sci. U.S.A. doi: 10.1073/pnas.90.12.5723 – volume: 278 start-page: 498 year: 2003 ident: 2021113010162211100_B15 article-title: Adipocyte-specific gene expression and adipogenic steatosis in the mouse liver due to peroxisome proliferator-activated receptor γ1 (PPARγ1) overexpression publication-title: J. Biol. Chem. doi: 10.1074/jbc.M210062200 – volume: 276 start-page: 38052 year: 2001 ident: 2021113010162211100_B7 article-title: Amino acid and insulin signaling via the mTOR/p70 S6 kinase pathway. A negative feedback mechanism leading to insulin resistance in skeletal muscle cells publication-title: J. Biol. Chem. doi: 10.1074/jbc.M106703200 – volume: 280 start-page: 22523 year: 2005 ident: 2021113010162211100_B11 article-title: PTEN, but not SHIP2, suppresses insulin signaling through the phosphatidylinositol 3-kinase/Akt pathway in 3T3-L1 adipocytes publication-title: J. Biol. Chem. doi: 10.1074/jbc.M501949200 – volume: 166 start-page: 213 year: 2004 ident: 2021113010162211100_B6 article-title: The TSC1-TSC2 tumor suppressor controls insulin-PI3K signaling via regulation of IRS proteins publication-title: J. Cell Biol. doi: 10.1083/jcb.200403069 – volume: 113 start-page: 1774 year: 2004 ident: 2021113010162211100_B12 article-title: Hepatocyte-specific Pten deficiency results in steatohepatitis and hepatocellular carcinomas publication-title: J. Clin. Invest. doi: 10.1172/JCI20513 – volume: 275 start-page: 12889 year: 2000 ident: 2021113010162211100_B8 article-title: The tumor suppressor PTEN negatively regulates insulin signaling in 3T3-L1 adipocytes publication-title: J. Biol. Chem. doi: 10.1074/jbc.275.17.12889 – year: 2009 ident: 2021113010162211100_B17 article-title: Maternal high-fat feeding primes steatohepatitis in adult mice offspring, involving mitochondrial dysfunction and altered lipogenesis gene expression publication-title: Hepatology doi: 10.1002/hep.23205 – volume: 112 start-page: 89 year: 2006 ident: 2021113010162211100_B3 article-title: PTEN and SHIP2 phosphoinositide phosphatases as negative regulators of insulin signalling publication-title: Arch. Physiol. Biochem. doi: 10.1080/13813450600711359 – volume: 134 start-page: 268 year: 2008 ident: 2021113010162211100_B4 article-title: PTEN down-regulation by unsaturated fatty acids triggers hepatic steatosis via an NF-κBp65/mTORdependent mechanism publication-title: Gastroenterology doi: 10.1053/j.gastro.2007.10.010 – volume: 36 start-page: 662 year: 2004 ident: 2021113010162211100_B10 article-title: Increase of PTEN gene expression in insulin resistance publication-title: Horm. Metab. Res. doi: 10.1055/s-2004-826016 – volume: 116 start-page: 539 year: 2009 ident: 2021113010162211100_B1 article-title: Metabolic disturbances in non-alcoholic fatty liver disease publication-title: Clin. Sci. doi: 10.1042/CS20080253 |
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| SubjectTerms | Animals Disease Progression Fatty Liver - etiology Female Hypoxia - complications Insulin Resistance Lipogenesis - genetics Mice PTEN Phosphohydrolase - deficiency |
| Title | Hypoxia and non-alcoholic fatty liver disease |
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