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Published on: February 19, 2019
Hepcidin is down-regulated in alcohol loading.
Takaaki Ohtake1, Hiroyuki Saito, Yayoi Hosoki
1Third Department of Internal Medicine, Asahikawa Medical College, Asahikawa 078-8510, Japan. totake@asahikawa-med.ac.jp
Alcoholism, Clinical and Experimental Research
|March 3, 2007
Summary
Alcohol consumption lowers hepcidin, a key hormone regulating iron. This down-regulation increases intestinal iron absorption, contributing to iron overload in alcoholic liver disease (ALD).
Area of Science:
- Hepatology
- Endocrinology
- Iron Metabolism
Background:
- Alcoholic liver disease (ALD) is associated with excess hepatic iron accumulation.
- The precise mechanism of hepatic iron uptake in ALD remains unclear.
- Hepcidin, an iron-regulatory hormone, controls iron absorption and macrophage release.
Purpose of the Study:
- To investigate the role of hepcidin in hepatic iron accumulation in ALD.
- To determine if alcohol loading affects hepcidin expression in ALD patients and a mouse model.
Main Methods:
- Serum prohepcidin quantified using ELISA.
- Hepatic hepcidin mRNA expression analyzed via qRT-PCR in mice.
- Prohepcidin protein expression assessed immunohistochemically in mouse liver.
Main Results:
- ALD patients exhibited significantly lower serum prohepcidin than healthy controls.
- Serum prohepcidin levels correlated inversely with serum ferritin in ALD patients.
- Ethanol feeding in mice reduced hepatic hepcidin-1 mRNA and prohepcidin protein expression.
Conclusions:
- Alcohol loading down-regulates hepatic hepcidin expression.
- Reduced hepcidin contributes to increased intestinal iron absorption in ALD.
- Hepcidin dysregulation plays a role in iron overload in alcoholic liver disease.
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