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Role of duodenal iron transporters and hepcidin in patients with alcoholic liver disease
Author(s) -
DostalikovaCimburova Marketa,
Balusikova Kamila,
Kratka Karolina,
Chmelikova Jitka,
Hejda Vaclav,
Hnanicek Jan,
Neubauerova Jitka,
Vranova Jana,
Kovar Jan,
Horak Jiri
Publication year - 2014
Publication title -
journal of cellular and molecular medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.44
H-Index - 130
eISSN - 1582-4934
pISSN - 1582-1838
DOI - 10.1111/jcmm.12310
Subject(s) - hepcidin , medicine , ferroportin , alcoholic liver disease , ferritin , endocrinology , western blot , duodenum , chemistry , dmt1 , gene expression , metabolism , transporter , anemia , biology , biochemistry , gene , cirrhosis
Patients with alcoholic liver disease ( ALD ) often display disturbed iron indices. Hepcidin, a key regulator of iron metabolism, has been shown to be down‐regulated by alcohol in cell lines and animal models. This down‐regulation led to increased duodenal iron transport and absorption in animals. In this study, we investigated gene expression of duodenal iron transport molecules and hepcidin in three groups of patients with ALD (with anaemia, with iron overload and without iron overload) and controls. Expression of DMT 1, FPN 1, DCYTB , HEPH , HFE and TFR 1 was measured in duodenal biopsies by using real‐time PCR and W estern blot. Serum hepcidin levels were measured by using ELISA . Serum hepcidin was decreased in patients with ALD . At the m RNA level, expressions of DMT 1 , FPN 1 and TFR 1 genes were significantly increased in ALD . This pattern was even more pronounced in the subgroups of patients without iron overload and with anaemia. Protein expression of FPN 1 paralleled the increase at the m RNA level in the group of patients with ALD . Serum ferritin was negatively correlated with DMT 1 m RNA . The down‐regulation of hepcidin expression leading to up‐regulation of iron transporters expression in the duodenum seems to explain iron metabolism disturbances in ALD . Alcohol consumption very probably causes suppression of hepcidin expression in patients with ALD .

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