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• W2088337621 endingPage "37" @default.
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• W2088337621 abstract "Abnormal accumulation of fat in the liver (steatosis) is commonly observed in hepatitis C virus (HCV) infection, and the severity of steatosis has been well correlated with the degree of hepatic fibrosis. In patients with chronic HCV infection, steatosis may occur in conjunction with other metabolic risk factors such as insulin resistance and the metabolic syndrome. This was observed primarily in patients infected with non-genotype 3 virus. Otherwise, in HCV-infected patients, especially those infected with genotype 3a, reductions in total cholesterol as well as high-density lipoprotein and low-density lipoprotein cholesterol are observed compared with matched controls, and the normalization of these parameters appears to be an important correlate of the response to antiviral therapy. In that setting, the pathogenic mechanisms involved in HCV-induced steatosis are mediated in large part by the HCV core protein, whose expression is associated with lipid droplet accumulation, changes in lipogenic gene expression and/or the activity of lipogenic proteins, and effects on mitochondrial oxidative function. The importance of genes such as peroxisome proliferator-activated receptor-α and the proteasome activator PA28-γ in HCV-mediated steatosis has been elucidated from studies in genetically altered mice, and the manipulation of these and other pathways may provide an avenue for therapeutic intervention." @default.
• W2088337621 created "2016-06-24" @default.
• W2088337621 creator A5026722725 @default.
• W2088337621 creator A5070639714 @default.
• W2088337621 date "2009-03-01" @default.
• W2088337621 modified "2023-10-03" @default.
• W2088337621 title "Hepatitis C virus, steatosis and lipid abnormalities: clinical and pathogenic data" @default.
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• W2088337621 doi "https://doi.org/10.1111/j.1478-3231.2008.01950.x" @default.
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