Duodenal expression of iron transport molecules in untreated haemochromatosis subjects
Background and aims: In HFE associated hereditary haemochromatosis, the duodenal enterocyte behaves as if iron deficient and previous reports have shown increased duodenal expression of divalent metal transporter 1 (DMT1) and iron regulated gene 1 (Ireg1) in affected subjects. In those studies, many...
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Published in | Gut Vol. 52; no. 7; pp. 953 - 959 |
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Main Authors | , , , , , , |
Format | Journal Article |
Language | English |
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01.07.2003
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Abstract | Background and aims: In HFE associated hereditary haemochromatosis, the duodenal enterocyte behaves as if iron deficient and previous reports have shown increased duodenal expression of divalent metal transporter 1 (DMT1) and iron regulated gene 1 (Ireg1) in affected subjects. In those studies, many patients had undergone venesection, which is a potent stimulus of iron absorption. Our study investigated duodenal expression of DMT1 (IRE and non-IRE), Ireg1, hephaestin, and duodenal cytochrome-b (Dyctb) in untreated C282Y homozygous haemochromatosis patients, iron deficient patients, and iron replete subjects. Methods: Total RNA was extracted from duodenal biopsies and expression of the iron transport genes was assessed by ribonuclease protection assay. Results: Expression of DMT1 (IRE) and Ireg1 was increased 3–5-fold in iron deficient subjects compared with iron replete subjects. Duodenal expression of DMT1 (IRE) and Ireg1 was similar in haemochromatosis patients and iron replete subjects but in haemochromatosis patients with elevated serum ferritin concentrations, both DMT1 (IRE) and Ireg1 expression were inappropriately increased relative to serum ferritin concentration. Hephaestin and Dcytb levels were not upregulated in haemochromatosis. DMT1 (IRE) and Ireg1 levels showed significant inverse correlations with serum ferritin concentration in each group of patients. Conclusions: These findings are consistent with DMT1 (IRE) and Ireg1 playing primary roles in the adaptive response to iron deficiency. Untreated haemochromatosis patients showed inappropriate increases in DMT1 (IRE) and Ireg1 expression for a given level of serum ferritin concentration, although the actual level of expression of these iron transport genes was not significantly different from that of normal subjects. |
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AbstractList | Background and aims: In HFE associated hereditary haemochromatosis, the duodenal enterocyte behaves as if iron deficient and previous reports have shown increased duodenal expression of divalent metal transporter 1 (DMT1 ) and iron regulated gene 1 (Ireg1 ) in affected subjects. In those studies, many patients had undergone venesection, which is a potent stimulus of iron absorption. Our study investigated duodenal expression of DMT1 (IRE and non-IRE ), Ireg1 , hephaestin , and duodenal cytochrome-b (Dyctb ) in untreated C282Y homozygous haemochromatosis patients, iron deficient patients, and iron replete subjects. Methods: Total RNA was extracted from duodenal biopsies and expression of the iron transport genes was assessed by ribonuclease protection assay. Results: Expression of DMT1 (IRE ) and Ireg1 was increased 3-5-fold in iron deficient subjects compared with iron replete subjects. Duodenal expression of DMT1 (IRE ) and Ireg1 was similar in haemochromatosis patients and iron replete subjects but in haemochromatosis patients with elevated serum ferritin concentrations, both DMT1 (IRE ) and Ireg1 expression were inappropriately increased relative to serum ferritin concentration. Hephaestin and Dcytb levels were not upregulated in haemochromatosis. DMT1 (IRE ) and Ireg1 levels showed significant inverse correlations with serum ferritin concentration in each group of patients. Conclusions: These findings are consistent with DMT1 (IRE ) and Ireg1 playing primary roles in the adaptive response to iron deficiency. Untreated haemochromatosis patients showed inappropriate increases in DMT1 (IRE ) and Ireg1 expression for a given level of serum ferritin concentration, although the actual level of expression of these iron transport genes was not significantly different from that of normal subjects. BACKGROUND AND AIMSIn HFE associated hereditary haemochromatosis, the duodenal enterocyte behaves as if iron deficient and previous reports have shown increased duodenal expression of divalent metal transporter 1 (DMT1) and iron regulated gene 1 (Ireg1) in affected subjects. In those studies, many patients had undergone venesection, which is a potent stimulus of iron absorption. Our study investigated duodenal expression of DMT1 (IRE and non-IRE), Ireg1, hephaestin, and duodenal cytochrome-b (Dyctb) in untreated C282Y homozygous haemochromatosis patients, iron deficient patients, and iron replete subjects.METHODSTotal RNA was extracted from duodenal biopsies and expression of the iron transport genes was assessed by ribonuclease protection assay.RESULTSExpression of DMT1 (IRE) and Ireg1 was increased 3-5-fold in iron deficient subjects compared with iron replete subjects. Duodenal expression of DMT1 (IRE) and Ireg1 was similar in haemochromatosis patients and iron replete subjects but in haemochromatosis patients with elevated serum ferritin concentrations, both DMT1 (IRE) and Ireg1 expression were inappropriately increased relative to serum ferritin concentration. Hephaestin and Dcytb levels were not upregulated in haemochromatosis. DMT1 (IRE) and Ireg1 levels showed significant inverse correlations with serum ferritin concentration in each group of patients.CONCLUSIONSThese findings are consistent with DMT1 (IRE) and Ireg1 playing primary roles in the adaptive response to iron deficiency. Untreated haemochromatosis patients showed inappropriate increases in DMT1 (IRE) and Ireg1 expression for a given level of serum ferritin concentration, although the actual level of expression of these iron transport genes was not significantly different from that of normal subjects. Background and aims: In HFE associated hereditary haemochromatosis, the duodenal enterocyte behaves as if iron deficient and previous reports have shown increased duodenal expression of divalent metal transporter 1 ( DMT1 ) and iron regulated gene 1 ( Ireg1 ) in affected subjects. In those studies, many patients had undergone venesection, which is a potent stimulus of iron absorption. Our study investigated duodenal expression of DMT1 ( IRE and non- IRE ), Ireg1 , hephaestin , and duodenal cytochrome-b ( Dyctb ) in untreated C282Y homozygous haemochromatosis patients, iron deficient patients, and iron replete subjects. Methods: Total RNA was extracted from duodenal biopsies and expression of the iron transport genes was assessed by ribonuclease protection assay. Results: Expression of DMT1 ( IRE ) and Ireg1 was increased 3–5-fold in iron deficient subjects compared with iron replete subjects. Duodenal expression of DMT1 ( IRE ) and Ireg1 was similar in haemochromatosis patients and iron replete subjects but in haemochromatosis patients with elevated serum ferritin concentrations, both DMT1 ( IRE ) and Ireg1 expression were inappropriately increased relative to serum ferritin concentration. Hephaestin and Dcytb levels were not upregulated in haemochromatosis. DMT1 ( IRE ) and Ireg1 levels showed significant inverse correlations with serum ferritin concentration in each group of patients. Conclusions: These findings are consistent with DMT1 ( IRE ) and Ireg1 playing primary roles in the adaptive response to iron deficiency. Untreated haemochromatosis patients showed inappropriate increases in DMT1 ( IRE ) and Ireg1 expression for a given level of serum ferritin concentration, although the actual level of expression of these iron transport genes was not significantly different from that of normal subjects. In HFE associated hereditary haemochromatosis, the duodenal enterocyte behaves as if iron deficient and previous reports have shown increased duodenal expression of divalent metal transporter 1 (DMT1) and iron regulated gene 1 (Ireg1) in affected subjects. In those studies, many patients had undergone venesection, which is a potent stimulus of iron absorption. Our study investigated duodenal expression of DMT1 (IRE and non-IRE), Ireg1, hephaestin, and duodenal cytochrome-b (Dyctb) in untreated C282Y homozygous haemochromatosis patients, iron deficient patients, and iron replete subjects. Total RNA was extracted from duodenal biopsies and expression of the iron transport genes was assessed by ribonuclease protection assay. Expression of DMT1 (IRE) and Ireg1 was increased 3-5-fold in iron deficient subjects compared with iron replete subjects. Duodenal expression of DMT1 (IRE) and Ireg1 was similar in haemochromatosis patients and iron replete subjects but in haemochromatosis patients with elevated serum ferritin concentrations, both DMT1 (IRE) and Ireg1 expression were inappropriately increased relative to serum ferritin concentration. Hephaestin and Dcytb levels were not upregulated in haemochromatosis. DMT1 (IRE) and Ireg1 levels showed significant inverse correlations with serum ferritin concentration in each group of patients. These findings are consistent with DMT1 (IRE) and Ireg1 playing primary roles in the adaptive response to iron deficiency. Untreated haemochromatosis patients showed inappropriate increases in DMT1 (IRE) and Ireg1 expression for a given level of serum ferritin concentration, although the actual level of expression of these iron transport genes was not significantly different from that of normal subjects. |
Author | Anderson, G J Stuart, K A Crawford, D H G McCullen, M Powell, L W Fletcher, L M Frazer, D M |
AuthorAffiliation | 1 Department of Gastroenterology and Hepatology, Princess Alexandra Hospital, Brisbane, Australia 2 Iron Metabolism Laboratory, the Queensland Institute of Medical Research, Brisbane, Australia |
AuthorAffiliation_xml | – name: 2 Iron Metabolism Laboratory, the Queensland Institute of Medical Research, Brisbane, Australia – name: 1 Department of Gastroenterology and Hepatology, Princess Alexandra Hospital, Brisbane, Australia |
Author_xml | – sequence: 1 givenname: K A surname: Stuart fullname: Stuart, K A organization: Iron Metabolism Laboratory, the Queensland Institute of Medical Research, Brisbane, Australia – sequence: 2 givenname: G J surname: Anderson fullname: Anderson, G J organization: Iron Metabolism Laboratory, the Queensland Institute of Medical Research, Brisbane, Australia – sequence: 3 givenname: D M surname: Frazer fullname: Frazer, D M organization: Iron Metabolism Laboratory, the Queensland Institute of Medical Research, Brisbane, Australia – sequence: 4 givenname: L W surname: Powell fullname: Powell, L W organization: Iron Metabolism Laboratory, the Queensland Institute of Medical Research, Brisbane, Australia – sequence: 5 givenname: M surname: McCullen fullname: McCullen, M organization: Iron Metabolism Laboratory, the Queensland Institute of Medical Research, Brisbane, Australia – sequence: 6 givenname: L M surname: Fletcher fullname: Fletcher, L M organization: Iron Metabolism Laboratory, the Queensland Institute of Medical Research, Brisbane, Australia – sequence: 7 givenname: D H G surname: Crawford fullname: Crawford, D H G organization: Iron Metabolism Laboratory, the Queensland Institute of Medical Research, Brisbane, Australia |
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Keywords | Human Immunopathology Hemochromatosis Duodenal disease Duodenum Metabolic diseases Iron Gene expression Hereditary Enzymopathy Molecules Messenger RNA Biopsy Clinical biology Digestive diseases Genetics Transport |
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Notes | istex:D489BEE8B55FB1391B78CB0B813AE6DC9D9D5C43 PMID:12801950 ark:/67375/NVC-64PFGXZZ-V Correspondence to: Dr K Stuart, Department of Gastroenterology and Hepatology, Princess Alexandra Hospital, Ipswich Rd, Woolloongabba, 4102 QLD, Australia; Drkastuart@AOL.com local:0520953 href:gutjnl-52-953.pdf ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 Correspondence to: Dr K Stuart, Department of Gastroenterology and Hepatology, Princess Alexandra Hospital, Ipswich Rd, Woolloongabba, 4102 QLD, Australia; Drkastuart@AOL.com |
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Snippet | Background and aims: In HFE associated hereditary haemochromatosis, the duodenal enterocyte behaves as if iron deficient and previous reports have shown... In HFE associated hereditary haemochromatosis, the duodenal enterocyte behaves as if iron deficient and previous reports have shown increased duodenal... BACKGROUND AND AIMSIn HFE associated hereditary haemochromatosis, the duodenal enterocyte behaves as if iron deficient and previous reports have shown... Background and aims: In HFE associated hereditary haemochromatosis, the duodenal enterocyte behaves as if iron deficient and previous reports have shown... |
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SubjectTerms | Adolescent Adult Aged Biological and medical sciences Biological Transport - physiology Biopsy Cation Transport Proteins - analysis Cytochrome b Group - analysis Dcytb divalent metal transporter 1 DMT1 duodenal cytochrome-b Duodenum - metabolism Enzymes Female Ferritins - blood GAPDH Genes glyceraldehyde-3-phosphate dehydrogenase haemochromatosis Hemochromatosis - metabolism hephaestin hereditary haemochromatosis HHC Hospitals Humans IRE Ireg1 Iron iron deficiency iron regulated gene 1 iron responsive element Iron-Binding Proteins - analysis Iron-Binding Proteins - blood Iron-Binding Proteins - metabolism Iron-Regulatory Proteins - genetics Male Medical research Medical sciences Membrane Proteins - analysis Metabolic diseases Metals (hemochromatosis...) Middle Aged Mutation Other metabolic disorders Proteins ribonuclease protection assay RNA - analysis Rodents RPA serum ferritin concentration Small Intestine Studies transferrin saturation untranslated region Up-Regulation - physiology UTR |
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Title | Duodenal expression of iron transport molecules in untreated haemochromatosis subjects |
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