Open AccessInsulin resistance and liver steatosis in chronic hepatitis C infection genotype 3
Author(s) -
Ludovico Abenavoli,
Mario Masarone,
Valentina Peta,
Nataša Milić,
Nazarii Kobyliak,
Samir Rouabhia,
Marcello Persico
Publication year - 2014
Publication title -
world journal of gastroenterology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.427
H-Index - 155
eISSN - 2219-2840
pISSN - 1007-9327
DOI - 10.3748/wjg.v20.i41.15233
Subject(s) - steatosis , insulin resistance , fatty liver , hepatitis c virus , genotype , medicine , liver disease , hepatitis c , viral load , immunology , ribavirin , virus , virology , biology , disease , insulin , gene , biochemistry
Hepatitis C virus (HCV) infection is a common chronic liver disease worldwide. Non-alcoholic fatty liver disease and insulin resistance (IR) are the major determinants of fibrosis progression and response to antiviral therapy. The pathogenetic link between IR and chronic HCV infection is complex, and is associated with HCV genotype. Liver steatosis is the most common in the patients infected with genotype 3 virus, possibly due to direct effects of genotype 3 viral proteins. To the contrary, hepatic steatosis in the patients infected with other genotypes is thought to be mostly due to the changes in host metabolism, involving IR. In HCV genotype 3, liver steatosis correlates with viral load, reverts after reaching the sustained virologic response and reoccurs in the relapsers. A therapeutic strategy to improve IR and liver steatosis and subsequently the response to antiviral treatment in these patients is warranted.