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A step closer to understanding fatty liver due to HCV
Chronic hepatitis C virus (HCV) infection afflicts about 200 million people worldwide and is presently the most common cause of cirrhosis and hepatocellular carcinoma in Western countries. Over the last decade, an association between HCV infection, hepatic steatosis, insulin resistance (IR) and type II diabetes has been highlighted, although the cause–effect relationship underlying the co-existence of these phenomena has yet to be completely clarified.1 These observations are important because the presence of steatosis and/or IR in chronic HCV infection appears to modulate the progression of fibrosis and the response to antiviral therapy in chronic HCV infection.2–4
Mechanisms underling steatosis development in chronic HCV infection have been demonstrated to be genotype specific, with an apparent direct steatogenic effect of genotype 3, and an IR-associated steatosis effect exerted by genotype 1.5,6 The direct steatogenic effect of HCV genotype 3 is confirmed by findings such as those showing a correlation between HCV genotype 3 RNA level and steatosis in chronically infected patients and the resolution of steatosis in genotype 3-infected patients after response to antiviral treatment.5–7
Several mechanisms whereby HCV infection can directly cause steatosis have been described. HCV can affect de novo fatty acid biosynthesis, triglyceride (TG) assembly and secretion, and lipid peroxidation. HCV core protein has also been shown to localise in the periphery of TG-rich lipid droplets and on the cytosolic surface of the endoplasmic reticulum (ER) membrane, and it might physically interfere with lipids and other proteins involved in very low-density lipoprotein (VLDL) assembly.8 Lipid secretion can be altered by the effect of HCV on microsomal triglyceride transfer protein (MTP) and apolipoproteins. MTP is an enzyme that regulates VLDL assembly and its activity is impaired by HCV core protein in core-transgenic …
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