Observational Study
Copyright ©The Author(s) 2016. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Hepatol. Jan 8, 2016; 8(1): 74-82
Published online Jan 8, 2016. doi: 10.4254/wjh.v8.i1.74
Adipokines, cytokines and body fat stores in hepatitis C virus liver steatosis
Emilio González-Reimers, Javier López-Prieto, Geraldine Quintero-Platt, Ricardo Pelazas-González, M Remedios Alemán-Valls, Onán Pérez-Hernández, M José de-la-Vega-Prieto, M Angeles Gómez-Rodríguez, Candelaria Martín-González, Francisco Santolaria-Fernández
Emilio González-Reimers, Javier López-Prieto, Geraldine Quintero-Platt, Ricardo Pelazas-González, M Remedios Alemán-Valls, Onán Pérez-Hernández, M José de-la-Vega-Prieto, M Angeles Gómez-Rodríguez, Candelaria Martín-González, Francisco Santolaria-Fernández, Servicio de Medicina Interna, Hospital Universitario de Canarias, Universidad de La Laguna, 38320 Canary Islands, Spain
Author contributions: González-Reimers E, López-Prieto J, Quintero-Platt G, Pelazas-González R, Alemán-Valls MR, Pérez-Hernández O, Martín-González C contributed to study conception and design; González-Reimers E, López-Prieto J, Quintero-Platt G, Alemán-Valls MR and Santolaria-Fernández F contributed to data acquisition, data analysis and interpretation, and writing of the article; López-Prieto J, Pelazas-González R and Pérez-Hernández O contributed to histomorphometrical analysis of the liver biopsies; de-la-Vega-Prieto MJ contributed to determination of cytokines and adipokines; Gómez-Rodríguez MA contributed to data acquisition and analysis of body composition by densitometry.
Institutional review board statement: The study was reviewed and approved by the Ethics Committee of the Hospital Universitario de Canarias (PI/07) and the Institutional Review Board from the third cycle studies of the University of la Laguna.
Informed consent statement: All the patients provided written informed consent before starting the study procedures.
Conflict-of-interest statement: The authors declare that there is no conflict of interest regarding this manuscript. No funding or institutional grants have been received for this study.
Data sharing statement: They are available upon request by emailing egonrey@ull.es. There is no written informed consent for data sharing, but data are anonymized.
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: Emilio González-Reimers, PhD, Servicio de Medicina Interna, Hospital Universitario de Canarias, Universidad de La Laguna, Ofra s/n, San Cristóbal de La Laguna, Tenerife, 38320 Canary Islands, Spain. egonrey@ull.es
Telephone: +34-92-2678600
Received: July 30, 2015
Peer-review started: July 31, 2015
First decision: September 29, 2015
Revised: October 19, 2015
Accepted: December 18, 2015
Article in press: December 21, 2015
Published online: January 8, 2016
Processing time: 161 Days and 21.4 Hours
Abstract

AIM: To identify patients with or without liver steatosis and its severity in treatment-naïve patients affected by hepatitis C virus (HCV) infection.

METHODS: We included 56 HCV infected patients, and assessed the amount of liver fat by histomorphometry, and its relationships with fat and lean mass at different parts of the body (by densitometry), hormones [insulin, homeostatic model assessment (HOMA)], adipokines (resistin, adiponectin, leptin), and cytokines (tumor necrosis factor α, interleukin-6).

RESULTS: Although the intensity of liver steatosis is related to trunk fat mass and HOMA, 33% of patients showed no liver steatosis, and this finding was not related to body mass index or genotype. Besides trunk fat mass, no other factor was related to the presence or not of liver steatosis, or to the intensity of it, by multivariate analysis. Lean mass was not related to liver steatosis. Adiponectin levels were lower among patients. No differences were observed in leptin and resistin.

CONCLUSION: Steatosis in HCV infection is common (67.2%), and closely related to trunk fat, and insulin resistance, but not with leg fat mass or adipokines.

Keywords: Resistin; Adiponectin; Insulin resistance; Proinflammatory cytokines; Leptin; Hepatitis C virus; Liver steatosis

Core tip: Pathogenesis of liver steatosis in hepatitis C virus (HCV) infection is complex and is not fully understood. For unknown reasons some patients, despite having a high body mass index (BMI), do not develop liver steatosis, whereas others with normal BMI develop intense liver fat deposition. We analyse if body fat and lean mass composition, insulin resistance and adipokine profile may help to identify patients with or without liver steatosis and its severity in treatment-naïve HCV patients. Multivariate analysis showed that only trunk fat mass and insulin resistance were independently related to liver steatosis assessed on histomorphometrical grounds and its severity.