©The Author(s) 2017. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Hepatol. Mar 18, 2017; 9(8): 443-454
Published online Mar 18, 2017. doi: 10.4254/wjh.v9.i8.443
Published online Mar 18, 2017. doi: 10.4254/wjh.v9.i8.443
Meta-analysis reveals up-regulation of cholesterol processes in non-alcoholic and down-regulation in alcoholic fatty liver disease
Wasco Wruck, James Adjaye, Medical Faculty, Institute for Stem Cell Research and Regenerative Medicine, Heinrich Heine University, 40225 Düsseldorf, Germany
Author contributions: Wruck W performed transcriptomics analyses and the meta-analysis; Wruck W and Adjaye J wrote the manuscript; Adjaye J initiated and co-ordinated the work.
Supported by The Medical Faculty of the Heinrich Heine University Düsseldorf .
Conflict-of-interest statement: The authors have no conflict of interest.
Data sharing statement: No additional data are available.
Correspondence to: James Adjaye, PhD, Professor, Medical Faculty, Institute for Stem Cell Research and Regenerative Medicine, Heinrich Heine University, Moorenstrasse 5, 40225 Düsseldorf, Germany. james.adjaye@med.uni-duesseldorf.de
Telephone: +49-0211-8108191 Fax: +49-0211-8117858
Received: October 12, 2016
Peer-review started: October 17, 2016
First decision: November 14, 2016
Revised: November 29, 2016
Accepted: December 13, 2016
Article in press: December 14, 2016
Published online: March 18, 2017
Processing time: 152 Days and 11.3 Hours
Peer-review started: October 17, 2016
First decision: November 14, 2016
Revised: November 29, 2016
Accepted: December 13, 2016
Article in press: December 14, 2016
Published online: March 18, 2017
Processing time: 152 Days and 11.3 Hours
Core Tip
Core tip: With a meta-analysis of newly published liver biopsy-derived transcriptome datasets we identified multiple key genes and pathways in common and mutually exclusive in alcoholic liver disease (ALD) and non-alcoholic fatty liver disease (NAFLD). We provide a compendium of comparative regulation for all KEGG pathways in both diseases and propose a list of biomarkers distinguishing both diseases. One surprising finding was that cholesterol metabolism was up-regulated in NAFLD and down-regulated in ALD although leading to the same steatosis phenotype which might be explained by an insufficient conversion rate to bile acids under both conditions.