Copyright ©2014 Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. Nov 7, 2014; 20(41): 15233-15240
Published online Nov 7, 2014. doi: 10.3748/wjg.v20.i41.15233
Insulin resistance and liver steatosis in chronic hepatitis C infection genotype 3
Ludovico Abenavoli, Mario Masarone, Valentina Peta, Natasa Milic, Nazarii Kobyliak, Samir Rouabhia, Marcello Persico
Ludovico Abenavoli, Valentina Peta, Department of Health Sciences, University Magna Græcia, 88100 Catanzaro, Italy
Mario Masarone, Marcello Persico, Internal Medicine and Hepatology Unit, University of Salerno, 84081 Baronissi, Italy
Natasa Milic, Department of Pharmacy, University of Novi Sad, 21000 Novi Sad, Serbia
Nazarii Kobyliak, Bogomolets National Medical University, 01601 Kiev, Ukraine
Samir Rouabhia, Department of Internal Medicine, University Hospital Center Touhami Benfis, Batna 05000, Algeria
Author contributions: Abenavoli L designed the paper, performed research of literature data and wrote the paper; Masarone M performed research of literature data and wrote the paper; Peta V, Kobyliak N and Rouabhia S critically revised the paper; Milic N performed research of literature data and revised the paper; Persico M analysed data and drafted the article.
Correspondence to: Ludovico Abenavoli, MD, PhD, Department of Health Sciences, University Magna Græcia, Campus Germaneto, Viale Europa, 88100 Catanzaro, Italy.
Telephone: +39-961-3694387 Fax: +39-961-754220
Received: March 18, 2014
Revised: April 28, 2014
Accepted: June 12, 2014
Published online: November 7, 2014

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.

Keywords: Insulin resistance, Non-alcoholic fatty liver disease, Hepatitis C virus, Genotype 3, Sustained virological response

Core tip: Three main types of steatosis in the patients with Hepatitis C virus (HCV) infection are known: a metabolic type associated with metabolic syndrome and two viral types: one that seems to be directly triggered by the virus and one that could originate from the interference of the virus in the mechanisms of insulin resistance. The first viral type is particularly widely considered to be predominant and, perhaps, strictly linked to HCV genotype 3 infection and its intra-hepatic viral load. This evidence is supported by the resolution of steatosis in most patients infected with genotype 3 virus after HCV eradication by antiviral therapy.