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Statements

Subject Item
n2:RIV%2F00216208%3A11120%2F14%3A43908521%21RIV15-MSM-11120___
rdf:type
skos:Concept n16:Vysledek
dcterms:description
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 DMT1, FPN1, DCYTB, HEPH, HFE and TFR1 was measured in duodenal biopsies by using real-time PCR and Western blot. Serum hepcidin levels were measured by using ELISA. Serum hepcidin was decreased in patients with ALD. At the mRNA level, expressions of DMT1, FPN1 and TFR1 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 FPN1 paralleled the increase at the mRNA level in the group of patients with ALD. Serum ferritin was negatively correlated with DMT1 mRNA. 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. 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 DMT1, FPN1, DCYTB, HEPH, HFE and TFR1 was measured in duodenal biopsies by using real-time PCR and Western blot. Serum hepcidin levels were measured by using ELISA. Serum hepcidin was decreased in patients with ALD. At the mRNA level, expressions of DMT1, FPN1 and TFR1 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 FPN1 paralleled the increase at the mRNA level in the group of patients with ALD. Serum ferritin was negatively correlated with DMT1 mRNA. 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.
dcterms:title
Role of duodenal iron transporters and hepcidin in patients with alcoholic liver disease Role of duodenal iron transporters and hepcidin in patients with alcoholic liver disease
skos:prefLabel
Role of duodenal iron transporters and hepcidin in patients with alcoholic liver disease Role of duodenal iron transporters and hepcidin in patients with alcoholic liver disease
skos:notation
RIV/00216208:11120/14:43908521!RIV15-MSM-11120___
n3:aktivita
n7:I n7:Z
n3:aktivity
I, Z(MSM0021620814)
n3:cisloPeriodika
9
n3:dodaniDat
n13:2015
n3:domaciTvurceVysledku
n4:1758330 n4:6151388 n4:9352163 n4:1579630 n4:9980245 n4:1217941 n4:5621879 n4:3566447 n4:1116339 n4:7090277
n3:druhVysledku
n19:J
n3:duvernostUdaju
n12:S
n3:entitaPredkladatele
n11:predkladatel
n3:idSjednocenehoVysledku
43105
n3:idVysledku
RIV/00216208:11120/14:43908521
n3:jazykVysledku
n18:eng
n3:klicovaSlova
gene expression; iron; alcoholic liver disease; hepcidin; HFE; TFR1; HEPH; DCYTB; FPN1; DMT1
n3:klicoveSlovo
n5:DCYTB n5:HEPH n5:DMT1 n5:alcoholic%20liver%20disease n5:HFE n5:FPN1 n5:iron n5:TFR1 n5:hepcidin n5:gene%20expression
n3:kodStatuVydavatele
GB - Spojené království Velké Británie a Severního Irska
n3:kontrolniKodProRIV
[00B071725255]
n3:nazevZdroje
Journal of Cellular and Molecular Medicine
n3:obor
n9:EB
n3:pocetDomacichTvurcuVysledku
10
n3:pocetTvurcuVysledku
10
n3:rokUplatneniVysledku
n13:2014
n3:svazekPeriodika
18
n3:tvurceVysledku
Krátká, Karolína Vránová, Jana Dostalíková-Čimburová, Markéta Hnaníček, Jan Neubauerová, Jitka Balušíková, Kamila Hejda, Václav Kovář, Jan Horák, Jiří Chmelíková, Jitka
n3:wos
000342980100014
n3:zamer
n14:MSM0021620814
s:issn
1582-1838
s:numberOfPages
11
n17:doi
10.1111/jcmm.12310
n15:organizacniJednotka
11120