Hypoxia and non-alcoholic fatty liver disease

被引:28
作者
Byrne, Christopher D. [1 ]
机构
[1] Univ Southampton, Southampton Gen Hosp, Inst Dev Sci, Dept Endocrinol & Metab, Southampton S016 6YD, Hants, England
关键词
beta-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); 3T3-L1; ADIPOCYTES; INSULIN-RESISTANCE; GENE-EXPRESSION; PTEN; STEATOHEPATITIS; STEATOSIS; MECHANISM; PATHWAY; SHIP2;
D O I
10.1042/CS20090565
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
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.
引用
收藏
页码:397 / 400
页数:4
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