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.<br/><br/>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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