Hepatitis C virus, steatosis and lipid abnormalities: clinical and pathogenic data. Export

@article{citeulike:6066255, 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-alpha and the proteasome activator PA28-gamma 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.}, author = {Negro, Francesco and Sanyal, Arun J.}, citeulike-article-id = {6066255}, citeulike-linkout-0 = {http://dx.doi.org/10.1111/j.1478-3231.2008.01950.x}, citeulike-linkout-1 = {http://view.ncbi.nlm.nih.gov/pubmed/19187070}, citeulike-linkout-2 = {http://www.hubmed.org/display.cgi?uids=19187070}, doi = {10.1111/j.1478-3231.2008.01950.x}, issn = {1478-3231}, journal = {Liver international : official journal of the International Association for the Study of the Liver}, keywords = {hcv, nash}, month = {March}, pages = {26--37}, posted-at = {2009-11-04 04:08:59}, priority = {2}, title = {Hepatitis C virus, steatosis and lipid abnormalities: clinical and pathogenic data.}, url = {http://dx.doi.org/10.1111/j.1478-3231.2008.01950.x}, volume = {29 Suppl 2}, year = {2009} }

TY - JOUR ID - citeulike:6066255 L3 - citeulike-article-id:6066255 N2 - 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-alpha and the proteasome activator PA28-gamma 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. JF - Liver international : official journal of the International Association for the Study of the Liver SN - 1478-3231 EP - 37 TI - Hepatitis C virus, steatosis and lipid abnormalities: clinical and pathogenic data. VL - 29 Suppl 2 SP - 26 KW - hcv KW - nash AU - Negro, Francesco AU - Sanyal, Arun PY - 2009/03// UR - http://dx.doi.org/10.1111/j.1478-3231.2008.01950.x ER -