Hepatitis C virus core protein modulates fatty acid metabolism and thereby causes lipid accumulation in the liver

We studied the roles of hepatitis C virus (HCV) core protein in hepatic steatosis and changes in hepatic lipid metabolism. HCV core protein expression plasmid was transfected in HepG2. Triacylglyceride (TG) and mRNA level associated with lipid metabolism were measured. Male C57BL/6 mice were infecte...

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Bibliographic Details
Published in:Digestive diseases and sciences 2005-07, Vol.50 (7), p.1361-1371
Main Authors: YAMAGUCHI, Atsushi, TAZUMA, Susumu, NISHIOKA, Tomoji, OHISHI, Waka, HYOGO, Hideyuki, NOMURA, Shuichi, CHAYAMA, Kazuaki
Format: Article
Language:English
Subjects:
Adenovirus
Animals
Biological and medical sciences
Cell Line, Tumor
Fatty Acids - metabolism
Fatty Liver - metabolism
Gene Expression Regulation, Viral
Hepatitis C virus
Human viral diseases
Infectious diseases
Lipid Metabolism
Liver - metabolism
Male
Medical sciences
Mice
Mice, Inbred C57BL
Thiobarbituric Acid Reactive Substances - metabolism
Transfection
Triglycerides - metabolism
Viral Core Proteins - metabolism
Viral Core Proteins - physiology
Viral diseases
Viral hepatitis
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Summary:We studied the roles of hepatitis C virus (HCV) core protein in hepatic steatosis and changes in hepatic lipid metabolism. HCV core protein expression plasmid was transfected in HepG2. Triacylglyceride (TG) and mRNA level associated with lipid metabolism were measured. Male C57BL/6 mice were infected with HCV core recombinant adenovirus and used for lipids and mRNA studies. In HCV core protein-expressing cells, peroxisome proliferator-activated receptor (PPAR)alpha, multidrug resistance protein (MDR) 3, and microsomal triglyceride transfer protein (MTP) were down-regulated 48 hr after transfection. In HCV core protein-expressing mice, hepatic TG content and hepatic thiobarbituric acid-reactive substances increased. PPARalpha, MDR2, acyl-CoA oxidase (AOX), and carnitine palmitoyl transferase-1 (CPT-1) were down-regulated. HCV core protein down-regulated lipid metabolism-associated gene expression, Mdr2, CPT, and AOX, accompanied by down-regulation of PPARalpha. There findings may contribute to the understanding of HCV-related steatosis, induction of reactive oxygen species, and carcinogenesis.
ISSN:0163-2116
1573-2568
DOI:10.1007/s10620-005-2788-1