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Commentary. Hypoxia and non alcoholic fatty liver disease

Commentary. Hypoxia and non alcoholic fatty liver disease
Commentary. 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 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.

Abbreviations: CYP2E1, cytochrome P450 2E1; HIF-2?, hypoxia-induced factor-2?; mTOR, mammalian target of rapamycin; NAFLD, non-alcoholic fatty liver disease; NASH, non-alcoholic steatohepatitis; NEFA, non-esterified fatty acid (‘free fatty acid’); NF-?B, nuclear factor ?B; PI3K, phosphoinositide 3-kinase; PPAR-?, peroxisome-proliferator-activated receptor-?; PTEN, phosphatase and tensin homologue deleted on chromosome 10; SREBP-1c, sterol-regulatory-element-binding protein-1c.
?-oxidation, fatty liver, lipogenesis, non-alcoholic steatohepatitis (nash), peroxisome-proliferator-activated receptor (ppar), phosphatase and tensin homologue deleted on chromosome 10 (pten), sterol-regulatory-element-binding protein-1c (srebp-1c)
0143-5221
397-400
Byrne, C.D.
1370b997-cead-4229-83a7-53301ed2a43c
Byrne, C.D.
1370b997-cead-4229-83a7-53301ed2a43c

Byrne, C.D. (2010) Commentary. Hypoxia and non alcoholic fatty liver disease. Clinical Science, 118, 397-400. (doi:10.1042/CS20090565).

Record type: Article

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.

Abbreviations: CYP2E1, cytochrome P450 2E1; HIF-2?, hypoxia-induced factor-2?; mTOR, mammalian target of rapamycin; NAFLD, non-alcoholic fatty liver disease; NASH, non-alcoholic steatohepatitis; NEFA, non-esterified fatty acid (‘free fatty acid’); NF-?B, nuclear factor ?B; PI3K, phosphoinositide 3-kinase; PPAR-?, peroxisome-proliferator-activated receptor-?; PTEN, phosphatase and tensin homologue deleted on chromosome 10; SREBP-1c, sterol-regulatory-element-binding protein-1c.

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Published date: 2010
Keywords: ?-oxidation, fatty liver, lipogenesis, non-alcoholic steatohepatitis (nash), peroxisome-proliferator-activated receptor (ppar), phosphatase and tensin homologue deleted on chromosome 10 (pten), sterol-regulatory-element-binding protein-1c (srebp-1c)

Identifiers

Local EPrints ID: 72781
URI: https://eprints.soton.ac.uk/id/eprint/72781
ISSN: 0143-5221
PURE UUID: 1b8a13da-98bd-4980-ab9e-8cefb73dcce5
ORCID for C.D. Byrne: ORCID iD orcid.org/0000-0001-6322-7753

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Date deposited: 22 Feb 2010
Last modified: 15 Aug 2019 00:49

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