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Dysregulation of iron and copper homeostasis in nonalcoholic fatty liver.

Abstract

Elevated iron stores as indicated by hyperferritinemia with normal or mildly elevated transferrin saturation and mostly mild hepatic iron deposition are a characteristic finding in subjects with non-alcoholic fatty liver disease (NAFLD). Excess iron is observed in approximately one third of NAFLD patients and is commonly 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 which relates to the fact that excess iron catalyses the formation of toxic hydroxyl-radicals subsequently resulting in cellular damage. Iron removal improves insulin sensitivity, delays the onset of type 2 diabetes mellitus, improves pathologic liver function tests and likewise ameliorates NAFLD histology. Several mechanisms contribute to pathologic iron accumulation in NAFLD. These include impaired iron export from hepatocytes and mesenchymal Kupffer cells as a consequence of imbalances in the concentrations of iron regulatory factors, such as hepcidin, cytokines, copper or other dietary factors. This review summarizes the knowledge about iron homeostasis in NAFLD and the rationale for its therapeutic implications.

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  • Authors+Show Affiliations

    ,

    Elmar Aigner, Christian Datz, Obesity Research Unit, Paracelsus Medical University Salzburg, 5020 Salzburg, Austria.

    ,

    Elmar Aigner, Christian Datz, Obesity Research Unit, Paracelsus Medical University Salzburg, 5020 Salzburg, Austria.

    Elmar Aigner, Christian Datz, Obesity Research Unit, Paracelsus Medical University Salzburg, 5020 Salzburg, Austria.

    Source

    World journal of hepatology 7:2 2015 Feb 27 pg 177-88

    Pub Type(s)

    Journal Article
    Review

    Language

    eng

    PubMed ID

    25729473

    Citation

    Aigner, Elmar, et al. "Dysregulation of Iron and Copper Homeostasis in Nonalcoholic Fatty Liver." World Journal of Hepatology, vol. 7, no. 2, 2015, pp. 177-88.
    Aigner E, Weiss G, Datz C. Dysregulation of iron and copper homeostasis in nonalcoholic fatty liver. World J Hepatol. 2015;7(2):177-88.
    Aigner, E., Weiss, G., & Datz, C. (2015). Dysregulation of iron and copper homeostasis in nonalcoholic fatty liver. World Journal of Hepatology, 7(2), pp. 177-88. doi:10.4254/wjh.v7.i2.177.
    Aigner E, Weiss G, Datz C. Dysregulation of Iron and Copper Homeostasis in Nonalcoholic Fatty Liver. World J Hepatol. 2015 Feb 27;7(2):177-88. PubMed PMID: 25729473.
    * Article titles in AMA citation format should be in sentence-case
    TY - JOUR T1 - Dysregulation of iron and copper homeostasis in nonalcoholic fatty liver. AU - Aigner,Elmar, AU - Weiss,Günter, AU - Datz,Christian, PY - 2014/08/26/received PY - 2014/12/12/revised PY - 2014/12/29/accepted PY - 2015/3/3/entrez PY - 2015/3/3/pubmed PY - 2015/3/3/medline KW - Dysmetabolic iron overload syndrome KW - Hepcidin KW - Iron overload KW - Metabolic syndrome KW - Non-alcoholic fatty liver disease KW - Nonalcoholic steatohepatitis SP - 177 EP - 88 JF - World journal of hepatology JO - World J Hepatol VL - 7 IS - 2 N2 - Elevated iron stores as indicated by hyperferritinemia with normal or mildly elevated transferrin saturation and mostly mild hepatic iron deposition are a characteristic finding in subjects with non-alcoholic fatty liver disease (NAFLD). Excess iron is observed in approximately one third of NAFLD patients and is commonly 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 which relates to the fact that excess iron catalyses the formation of toxic hydroxyl-radicals subsequently resulting in cellular damage. Iron removal improves insulin sensitivity, delays the onset of type 2 diabetes mellitus, improves pathologic liver function tests and likewise ameliorates NAFLD histology. Several mechanisms contribute to pathologic iron accumulation in NAFLD. These include impaired iron export from hepatocytes and mesenchymal Kupffer cells as a consequence of imbalances in the concentrations of iron regulatory factors, such as hepcidin, cytokines, copper or other dietary factors. This review summarizes the knowledge about iron homeostasis in NAFLD and the rationale for its therapeutic implications. SN - 1948-5182 UR - https://www.unboundmedicine.com/medline/citation/25729473/full_citation L2 - http://www.wjgnet.com/1948-5182/full/v7/i2/177.htm DB - PRIME DP - Unbound Medicine ER -