Aigner E, Weiss G, Datz C. Dysregulation of iron and copper homeostasis in nonalcoholic fatty liver. World J Hepatol 2015; 7(2): 177-188 [PMID: 25729473 DOI: 10.4254/wjh.v7.i2.177]
Corresponding Author of This Article
Elmar Aigner, MD, First Department of Medicine, Paracelsus Private Medical University Salzburg, Müllner Hauptstrasse 48, 5020 Salzburg, Austria. e.aigner@salk.at
Research Domain of This Article
Gastroenterology & Hepatology
Article-Type of This Article
Review
Open-Access Policy of This Article
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/
World J Hepatol. Feb 27, 2015; 7(2): 177-188 Published online Feb 27, 2015. doi: 10.4254/wjh.v7.i2.177
Dysregulation of iron and copper homeostasis in nonalcoholic fatty liver
Elmar Aigner, Günter Weiss, Christian Datz
Elmar Aigner, Christian Datz, Obesity Research Unit, Paracelsus Medical University Salzburg, 5020 Salzburg, Austria
Elmar Aigner, First Department of Medicine, Paracelsus Medical University Salzburg, 5020 Salzburg, Austria
Günter Weiss, Department of Internal Medicine VI, Medical University Innsbruck, 6020 Innsbruck, Austria
Christian Datz, Department of Internal Medicine, General Hospital Oberndorf, 5111 Oberndorf, Austria
Author contributions: Aigner E drafted and finalized the manuscript; Weiss G and Datz C contributed to critical revision and important intellectual content.
Supported by PMU-Forschungsförderungsfonds, No. E-13/17/086-AIG; the Austrian Research Funds, FWF to Weiss G, Project TRP-188; and SPAR Austria to Christian Datz is gratefully acknowledged.
Conflict-of-interest: None of the authors has any potential financial conflicts of interest to disclose with regard to 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: Elmar Aigner, MD, First Department of Medicine, Paracelsus Private Medical University Salzburg, Müllner Hauptstrasse 48, 5020 Salzburg, Austria. e.aigner@salk.at
Telephone: +43-662-448258358 Fax: +43-662-4482881
Received: August 26, 2014 Peer-review started: August 27, 2014 First decision: November 27, 2014 Revised: December 12, 2014 Accepted: December 29, 2014 Article in press: December 31, 2014 Published online: February 27, 2015 Processing time: 170 Days and 9.8 Hours
Core Tip
Core tip: Hyperferritinemia with normal transferrin saturation and mostly mild hepatic iron deposition is a frequent finding in subjects with non-alcoholic fatty liver disease. Excess iron in non-alcoholic fatty liver disease (NAFLD) patients is referred to as the “dysmetabolic iron overload syndrome”. Clinical evidence suggests that elevated body iron stores aggravate the clinical course of NAFLD with regard to liver-related and extrahepatic disease complications. Iron removal improves insulin sensitivity, delays the onset of type 2 diabetes mellitus, improves pathologic liver function tests and ameliorates NAFLD histology The mechanisms contributing to iron excess in fatty liver include impaired iron export from hepatocytes and mesenchymal Kupffer.
