Role of alcohol in the regulation of iron metabolism
Open accessAbstract
Patients with alcoholic liver disease frequently exhibit increased body iron stores, as reflected by elevated serum iron indices (transferrin saturation, ferritin) and hepatic iron concentration. Even mild to moderate alcohol consumption has been shown to increase the prevalence of iron overload. Moreover, increased hepatic iron content is associated with greater mortality from alcoholic cirrhosis, suggesting a pathogenic role for iron in alcoholic liver disease. Alcohol increases the severity of disease in patients with genetic hemochromatosis, an iron overload disorder common in the Caucasian population. Both iron and alcohol individually cause oxidative stress and lipid peroxidation, which culminates in liver injury. Despite these observations, the underlying mechanisms of iron accumulation and the source of the excess iron observed in alcoholic liver disease remain unclear. Over the last decade, several novel iron-regulatory proteins have been identified and these have greatly enhanced our understanding of iron metabolism. For example, hepcidin, a circulatory antimicrobial peptide synthesized by the hepatocytes of the liver is now known to play a central role in the regulation of iron homeostasis. This review attempts to describe the interaction of alcohol and iron-regulatory molecules. Understanding these molecular mechanisms is of considerable clinical importance because both alcoholic liver disease and genetic hemochromatosis are common diseases, in which alcohol and iron appear to act synergistically to cause liver injury.
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Iron and alcohol together contribute to and aggravate liver disease.
“Thus iron and alcohol together contribute to and aggravate liver disease (Harrison-Findik, 2007).”
From Iron, Oxidative Stress and Health (2012) · cites this paper as Harrison-Findik, 2007
Glycosylated and oxidized proteins indirectly up-regulate CRP expression in hepatocytes by stimulating monocytes to produce IL-6.
“Glycosylated and oxidized proteins indirectly up-regulate CRP expression in hepatocytes by stimulating monocytes to produce IL-6 (Harrison-Findik, 2007).”
From Iron, Oxidative Stress and Health (2012) · cites this paper as Harrison-Findik, 2007
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- Authors
- Harrison-Findik, D. D.
- Affiliations
- Medical Research Foundation (GB)
- Corresponding author
- Harrison-Findik, Duygu Dee
- Venue
- World Journal of Gastroenterology
- Publisher
- Baishideng Publishing Group Inc.
- Published
- 2007
- Volume
- 13
- Issue
- 37
- Pages
- 4925
- ISSN
- 1007-9327 (ISSN-L)
- PMC
- PMC4434614
- OpenAlex
- W2404659621
- Cited by
- 156
- References
- 20
- Citations by year
- 2026: 10 · 2025: 7 · 2024: 10 · 2023: 11 · 2022: 17 · 2021: 7 · 2020: 5 · 2019: 3 · 2018: 3 · 2017: 4 · 2016: 4 · 2015: 2 · 2014: 12 · 2013: 9 · 2012: 9
- FWCI
- 7.28
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- World Journal of Gastroenterology (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Hematology › Iron Metabolism and Disorders
- Health Sciences › Medicine › Pathology and Forensic Medicine › Alcohol Consumption and Health Effects
- Health Sciences › Nursing › Nutrition and Dietetics › Trace Elements in Health
- Keywords
- alcohol, iron metabolism, alcoholic liver disease, iron overload, hemochromatosis, hepcidin, iron regulatory proteins, oxidative stress, lipid peroxidation, liver injury, alcoholic cirrhosis, hepatic iron deposition, transferrin saturation, ferritin
- MeSH terms
- Alcohol Drinking, Ethanol, Humans, Iron, Liver Diseases, Alcoholic, Iron Overload, Antimicrobial Cationic Peptides, Hepcidins
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