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©The Author(s) 2016. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Hepatol. Aug 28, 2016; 8(24): 1019-1027
Published online Aug 28, 2016. doi: 10.4254/wjh.v8.i24.1019
Published online Aug 28, 2016. doi: 10.4254/wjh.v8.i24.1019
Hypolactasia is associated with insulin resistance in nonalcoholic steatohepatitis
Daniel Ferraz de Campos Mazo, Rejane Mattar, José Tadeu Stefano, Joyce Matie Kinoshita da Silva-Etto, Márcio Augusto Diniz, Sebastião Mauro Bezerra Duarte, Fabíola Rabelo, Rodrigo Vieira Costa Lima, Priscila Brizolla de Campos, Flair José Carrilho, Claudia P Oliveira, Division of Gastroenterology and Hepatology, Department of Gastroenterology (LIM 07), University of São Paulo School of Medicine, São Paulo 05403-000, Brazil
Author contributions: de Campos Mazo DF, Mattar R and Oliveira CP conceived and designed the study, contributed to the data analysis and interpretation and wrote the manuscript; da Silva-Etto JMK and Mattar R performed the LCT-13910C>T genotyping; de Campos Mazo DF, Stefano JT, Duarte SMB, Rabelo F, Lima RVC and de Campos PB collected and assembled the data; Diniz MA performed the statistical analysis and analyzed the data; Carrilho FJ contributed to the data analysis and interpretation; all authors read and approved the final version of the manuscript.
Institutional review board statement: This study was conducted in accordance with the ethical guidelines of the 1975 Declaration of Helsinki and was approved by the Ethics Committee of the Hospital das Clínicas (No. 448520).
Informed consent statement: All involved persons provided their informed consent prior to study inclusion.
Conflict-of-interest statement: The authors declare no conflicts of interest in this work.
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: Claudia P Oliveira, MD, PhD, Division of Gastroenterology and Hepatology, Department of Gastroenterology (LIM 07), University of São Paulo School of Medicine, Av Dr Eneas de Carvalho Aguiar 255, 9° Andar, Sala 9159, São Paulo 05403-000, Brazil. cpm@.usp.br
Telephone: +55-11-26616447 Fax: +55-11-26617830
Received: April 26, 2016
Peer-review started: April 28, 2016
First decision: May 17, 2016
Revised: June 26, 2016
Accepted: July 14, 2016
Article in press: July 18, 2016
Published online: August 28, 2016
Peer-review started: April 28, 2016
First decision: May 17, 2016
Revised: June 26, 2016
Accepted: July 14, 2016
Article in press: July 18, 2016
Published online: August 28, 2016
Core Tip
Core tip: Non-alcoholic fatty liver disease (NAFLD) exhibits a close relationship with metabolic syndrome (MetS), but the associations of the lactase non-persistence/lactase persistence genotypes with MetS components are controversial. Therefore, we assessed hypolactasia (LCT-13910CC) and lactase persistence genotypes in 102 Brazilian NAFLD patients in comparison with 501 healthy controls, the associations of these polymorphisms were verified with the results of biochemical tests, MetS and severity of liver histology in nonalcoholic steatohepatitis (NASH) patients. No differences in the LCT-13910C>T polymorphisms were noted between the NAFLD and controls, but hypolactasia increased the risk of insulin resistance in the NASH patients.