Hepatitis C virus, insulin resistance, and steatosis

Kralj, Dominik and Virović Jukić, Lucija and Stojsavljević, Sanja and Duvnjak, Marko and Smolić, Martina and Bilić Čurčić, Ines (2016) Hepatitis C virus, insulin resistance, and steatosis. Journal of Clinical and Translational Hepatology, 4 (1). pp. 66-75. ISSN 2225-0719

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Abstract

Hepatitis C virus (HCV) is one of the main causes of liver disease worldwide. Liver steatosis is a common finding in many hepatic and extrahepatic disorders, the most common being metabolic syndrome (MS). Over time, it has been shown that the frequent coexistence of these two conditions is not coincidental, since many epidemiological, clinical, and experimental studies have indicated HCV to be strongly associated with liver steatosis and numerous metabolic derangements. Here, we present an overview of publications that provide clinical evidence of the metabolic effects of HCV and summarize the available data on the pathogenetic mechanisms of this association. It has been shown that HCV infection can induce insulin resistance (IR) in the liver and peripheral tissues through multiple mechanisms. Substantial research has suggested that HCV interferes with insulin signaling both directly and indirectly, inducing the production of several proinflammatory cytokines. HCV replication, assembly, and release from hepatocytes require close interactions with lipid droplets and host lipoproteins. This modulation of lipid metabolism in host cells can induce hepatic steatosis, which is more pronounced in patients with HCV genotype 3. The risk of steatosis depends on several viral factors (including genotype, viral load, and gene mutations) and host features (visceral obesity, type 2 diabetes mellitus, genetic predisposition, medication use, and alcohol consumption). HCV-related IR and steatosis have been shown to have a remarkable clinical impact on the prognosis of HCV infection and quality of life, due to their association with resistance to antiviral therapy, progression of hepatic fibrosis, and development of hepatocellular carcinoma. Finally, HCV-induced IR, oxidative stress, and changes in lipid and iron metabolism lead to glucose intolerance, arterial hypertension, hyperuricemia, and atherosclerosis, resulting in increased cardiovascular mortality.

Item Type: Article
Additional Information: © 2016 The Second Affiliated Hospital of Chongqing Medical University. Published by XIA & HE Publishing Inc. All rights reserved. This is an Open Access article distributed under the terms of the Creative Commons Attribution-Noncommercial 4.0 Unported License, permitting all non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
Departments: Katedra za internu medicinu
Depositing User: Marijan Šember
Status: Published
Creators:
CreatorsEmail
Kralj, DominikUNSPECIFIED
Virović Jukić, LucijaUNSPECIFIED
Stojsavljević, SanjaUNSPECIFIED
Duvnjak, MarkoUNSPECIFIED
Smolić, MartinaUNSPECIFIED
Bilić Čurčić, InesUNSPECIFIED
Date: 28 March 2016
Date Deposited: 23 May 2016 11:22
Last Modified: 23 May 2016 11:22
Subjects: /
Related URLs:
URI: http://medlib.mef.hr/id/eprint/2599

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