Abstract
Reduced low-density lipoprotein (LDL) cholesterol level is a characteristic feature of dyslipidemia in chronic hepatitis C virus (HCV) infection. However, abnormality in serum triglyceride (TG) has not been fully investigated. To clarify the impact of HCV genotype 1b (G1b) infection and advanced fibrosis on serum TG profiles, TG concentrations in lipoprotein fractions were examined in fasting sera from 185 subjects with active or cleared HCV infection by high-performance liquid chromatography. Serum lipoproteins were fractionated into four classes: chylomicron, very low-density lipoprotein (VLDL), LDL, and high-density lipoprotein (HDL). Then, the significance of HCV G1b infection on TG levels in each lipoprotein fraction was determined using multiple regression models. We found that active HCV G1b infection was positively associated with high HDL-TG levels and low VLDL-TG levels, independent of other factors included in the regression model. In VLDL sub-fractions, active HCV infection was only found to be associated with low levels of large VLDL-TG. Similarly, advanced liver fibrosis in chronic HCV G1b infection was associated with high levels of LDL-TG, HDL-TG, and small VLDL-TG, independent of other clinical factors. These findings indicate that active HCV G1b infection and advanced fibrosis are closely associated with abnormal serum TG profiles.
Highlights
Chronic hepatitis C virus (HCV) infection is a major health problem worldwide and a leading cause of liver cirrhosis and hepatic carcinogenesis
We found that an increase of low-density lipoprotein (LDL)-TG and small very-low-density lipoprotein (VLDL)-TG is an independent factor associated with chronic active HCV genotype 1b (G1b) infection with advanced fibrosis
Chronic active HCV G1b infection is associated with altered serum TG profiles, characterized by reduced levels of VLDL-TG and increased levels of high-density lipoprotein (HDL)-TG
Summary
Chronic hepatitis C virus (HCV) infection is a major health problem worldwide and a leading cause of liver cirrhosis and hepatic carcinogenesis. Alteration of lipid metabolism in HCV infection has been investigated, and it is clear that HCV infection predisposes an individual to dyslipidemia, and to hepatic steatosis [1] and advanced fibrosis. Many studies have reported abnormal serum lipid levels in HCV infection, especially low levels of total cholesterol (TC) [4] and low-density lipoprotein cholesterol (LDL-C) [5], little is known about the serum triglyceride (TG) profile in HCV infection. The liver, as a central organ in lipid metabolism, is involved in assembly and secretion of TG-rich very-low-density lipoprotein (VLDL) into circulation. VLDL is catabolized by lipoprotein lipase (LPL) to a VLDL remnant called intermediate density lipoprotein (IDL), which is further metabolized to LDL by hepatic triglyceride lipase (HTGL) or incorporated into hepatocytes
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