Retrospective Study
Copyright ©The Author(s) 2016. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Hepatol. Sep 8, 2016; 8(25): 1067-1074
Published online Sep 8, 2016. doi: 10.4254/wjh.v8.i25.1067
CD36 genetic variation, fat intake and liver fibrosis in chronic hepatitis C virus infection
Omar Ramos-Lopez, Sonia Roman, Erika Martinez-Lopez, Nora A Fierro, Karina Gonzalez-Aldaco, Alexis Jose-Abrego, Arturo Panduro
Omar Ramos-Lopez, Sonia Roman, Erika Martinez-Lopez, Nora A Fierro, Karina Gonzalez-Aldaco, Alexis Jose-Abrego, Arturo Panduro, Department of Molecular Biology in Medicine, Civil Hospital of Guadalajara “Fray Antonio Alcalde”, Guadalajara, Jalisco 44280, Mexico
Omar Ramos-Lopez, Sonia Roman, Erika Martinez-Lopez, Nora A Fierro, Karina Gonzalez-Aldaco, Alexis Jose-Abrego, Arturo Panduro, Health Sciences University Center, University of Guadalajara, Guadalajara, Jalisco 44340, Mexico
Author contributions: Ramos-Lopez O performed the genotyping experiments, statistical analysis and prepared the first draft of the manuscript; Roman S wrote, integrated the final version and critically revised the content of this article; Martinez-Lopez E provided the biochemical tests and critically revised the manuscript; Fierro NA wrote and critically revised the article; Gonzalez-Aldaco K and Jose-Abrego A wrote, revised statistical analysis and critically reviewed the manuscript; Panduro A conceived the study, performed clinical studies and transient elastography, wrote and critically revised the content of this article; all authors critically reviewed all drafts and approved the final manuscript.
Supported by Promep-University of Guadalajara to Arturo Panduro, No. UDG-CA-478.
Institutional review board statement: The study was reviewed and approved by the Ethics Committee of the Health Sciences University Center.
Informed consent statement: All study participants, or their legal guardian, provided informed written consent prior to study enrollment.
Conflict-of-interest statement: The authors declare that they have no conflict of interest.
Data sharing statement: No additional data are available.
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: Arturo Panduro, MD, PhD, FAASLD, Department of Molecular Biology in Medicine, Civil Hospital of Guadalajara “Fray Antonio Alcalde”, Hospital # 278, Col. El Retiro, Guadalajara, Jalisco 44280, Mexico. apanduro@prodigy.net.mx
Telephone: +52-33-36147743 Fax: +52-33-36147743
Received: March 29, 2016
Peer-review started: March 31, 2016
First decision: June 12, 2016
Revised: June 28, 2016
Accepted: August 11, 2016
Article in press: August 15, 2016
Published online: September 8, 2016
Processing time: 169 Days and 10.5 Hours
Abstract
AIM

To analyze the association of the CD36 polymorphism (rs1761667) with dietary intake and liver fibrosis (LF) in chronic hepatitis C (CHC) patients.

METHODS

In this study, 73 patients with CHC were recruited. The CD36 genotype (G > A) was determined by a TaqMan real-time PCR system. Dietary assessment was carried out using a three-day food record to register the daily intake of macronutrients. Serum lipids and liver enzymes were measured by a dry chemistry assay. LF evaluated by transient elastography (Fibroscan®) and APRI score was classified as mild LF (F1-F2) and advanced LF (F3-F4).

RESULTS

Overall, the CD36 genotypic frequencies were AA (30.1%), AG (54.8%), and GG (15.1%), whereas the allelic A and G frequencies were 57.5% and 42.5%, respectively. CHC patients who were carriers of the CD36 AA genotype had a higher intake of calories attributable to total fat and saturated fatty acids than those with the non-AA genotypes. Additionally, aspartate aminotransferase (AST) serum values were higher in AA genotype carriers compared to non-AA carriers (91.7 IU/L vs 69.8 IU/L, P = 0.02). Moreover, the AA genotype was associated with an increase of 30.23 IU/L of AST (β = 30.23, 95%CI: 9.0-51.46, P = 0.006). Likewise, the AA genotype was associated with advanced LF compared to the AG (OR = 3.60, 95%CI: 1.16-11.15, P = 0.02) or AG + GG genotypes (OR = 3.52, 95%CI: 1.18-10.45, P = 0.02).

CONCLUSION

This study suggests that the CD36 (rs1761667) AA genotype is associated with higher fat intake and more instances of advanced LF in CHC patients.

Keywords: Hepatitis C virus infection; CD36 receptor; Lipids; Liver fibrosis; Mexico

Core tip: In this study, chronically infected hepatitis C patients who were carriers of the AA genotype of the CD36 receptor polymorphism (rs1761667) showed a higher risk of advanced liver fibrosis compared to patients with an AG/GG genotype. This liver damage was associated with the consumption of a hepatopatogenic diet, high-calories and excessive intake of total and saturated fat, typical of the population of West Mexico. Thus, preventive nutritional intervention strategies based on the CD36 genotype may be a useful tool to avoid further liver damage due to alterations in liver lipid metabolism and inflammation in patients with chronic hepatitis C infection.