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Copyright ©The Author(s) 2015. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Hepatol. Jun 8, 2015; 7(10): 1337-1346
Published online Jun 8, 2015. doi: 10.4254/wjh.v7.i10.1337
Liver steatosis in hepatitis C patients
Emilio González-Reimers, Geraldine Quintero-Platt, Melchor Rodríguez-Gaspar, Remedios Alemán-Valls, Onán Pérez-Hernández, Francisco Santolaria-Fernández
Emilio González-Reimers, Geraldine Quintero-Platt, Melchor Rodríguez-Gaspar, Remedios Alemán-Valls, Onán Pérez-Hernández, Francisco Santolaria-Fernández, Servicio de Medicina Interna, Hospital Universitario de Canarias, Universidad de La Laguna, Tenerife, 38320 Canary Islands, Spain
Author contributions: González-Reimers E, Quintero-Platt G, Rodríguez-Gaspar M, Alemán-Valls R, Pérez-Hernández O and Santolaria-Fernández F contributed to the review of the literature; González-Reimers E and Quintero-Platt G contributed to the drafting of the manuscript.
Conflict-of-interest: The authors declare that there is no conflict of interest regarding this manuscript.
Open-Access: This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
Correspondence to: Dr. Emilio González-Reimers, Servicio de Medicina Interna, Hospital Universitario de Canarias, Universidad de La Laguna, Ofra s/n, Tenerife, 38320 Canary Islands, Spain. egonrey@ull.es
Telephone: +34-922-678600
Received: July 31, 2014
Peer-review started: August 1, 2014
First decision: September 16, 2014
Revised: February 8, 2015
Accepted: March 5, 2015
Article in press: March 9, 2015
Published online: June 8, 2015
Abstract

There is controversy regarding some aspects of hepatitis C virus (HCV) infection-associated liver steatosis, and their relationship with body fat stores. It has classically been found that HCV, especially genotype 3, exerts direct metabolic effects which lead to liver steatosis. This supports the existence of a so called viral steatosis and a metabolic steatosis, which would affect HCV patients who are also obese or diabetics. In fact, several genotypes exert metabolic effects which overlap with some of those observed in the metabolic syndrome. In this review we will analyse the pathogenic pathways involved in the development of steatosis in HCV patients. Several cytokines and adipokines also become activated and are involved in “pure” steatosic effects, in addition to inflammation. They are probably responsible for the evolution of simple steatosis to steatohepatitis, making it difficult to explain why such alterations only affect a proportion of steatosic patients.

Keywords: Hepatitis C virus steatosis adiponectin, Leptin, Insulin resistance, Proinflammatory cytokines, Triglyceride synthesis, Fatty acid oxidation

Core tip: Chronic hepatitis C virus (HCV) infection can lead to steatosis and steatohepatitis. Increased liver triglyceride synthesis is mediated by several transcription factors such as sterol regulatory element-binding protein (SREBP) whose expression is enhanced, in turn, by HCV core protein. Chronic HCV infection is also associated with insulin resistance that seems to be selective because although it activates systemic lipolysis, it increases triglyceride synthesis within the liver. This is due to the stimulatory effect of insulin on SREBP. It remains to be answered why not all patients with HCV infection and steatosis develop steatohepatitis despite early cytokine activation and metabolic derangements.