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Iron Perturbations in Human Non-Alcoholic Fatty Liver Disease (NAFLD): Clinical Relevance and Molecular Mechanisms

AUTHORS

Elmar Aigner 1 , Christian Datz 2 , *

AUTHORS INFORMATION

1 Department of Internal Medicine, General Hospital of Oberndorf, Austria

2 Department of Internal Medicine, General Hospital of Oberndorf, c.datz@kh-obdf.salzburg.at, Austria

How to Cite: Aigner E, Datz C. Iron Perturbations in Human Non-Alcoholic Fatty Liver Disease (NAFLD): Clinical Relevance and Molecular Mechanisms, Hepat Mon. Online ahead of Print ; 8(3):213-220.

ARTICLE INFORMATION

Hepatitis Monthly: 8 (3); 213-220
Article Type: Review Article
Received: March 19, 2007
Accepted: August 18, 2007

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Abstract

Non-alcoholic fatty liver disease (NAFLD) is the hepatic manifestation of the insulin resistance syndrome and thus a frequent cause of elevated liver enzymes. The term "insulin-resistance associated hepatic iron overload syndrome (IR-HIOS)" has been coined to describe the frequent association of hepatic steatosis with increased levels of serum ferritin, normal or slightly elevated transferrin saturation and mild hepatic iron deposition. There is mounting evidence that increased iron stores in insulin resistance are associated with an unfavorable course of the disease and an increased prevalence of associated conditions such as diabetes, hypertension or cardiovascular disease. Iron depletion via phlebotomy has been demonstrated to improve several aspects of the insulin-resistance syndrome. Multiple interactions have been observed between molecules of iron and glucose metabolism. On a molecular level, impaired iron export has been demonstrated to be the principal mechanism of iron accumulation in fatty liver disease. Obesity-related inflammation, low ferroxidase activity associated with low copper bioavailability and decreased expression of the iron export molecule ferroportein have so far been identified as contributors to increased iron accumulation in human NAFLD.

Keywords

Non-Alcoholic Fatty Liver Disease Iron Overload Insulin Resistance

© 0, Author(s). This is an open-access article distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 International License (http://creativecommons.org/licenses/by-nc/4.0/) which permits copy and redistribute the material just in noncommercial usages, provided the original work is properly cited.

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