Journal
CLINICAL SCIENCE
Volume 118, Issue 5-6, Pages 397-400Publisher
PORTLAND PRESS LTD
DOI: 10.1042/CS20090565
Keywords
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)
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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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