| Hepcidin response to acute iron intake and chronic iron loading in dysmetabolic iron overload syndrome. | |
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MedLine Citation:
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PMID: 21733088 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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BACKGROUND: The pathogenesis of dysmetabolic iron overload syndrome (DIOS) is still unclear. Hepcidin is the key regulator of iron homeostasis controlling iron absorption and macrophage release. AIM: To investigate hepcidin regulation by iron in DIOS. METHODS: We analysed urinary hepcidin at baseline and 24 h after a 65 mg oral iron dose in 24 patients at diagnosis and after iron depletion (n = 13) and compared data with those previously observed in 23 healthy controls. Serum iron indices, liver histology and metabolic data were available for all patients. RESULTS: At diagnosis, hepcidin values were significantly higher than in controls (P < 0.001). After iron depletion, hepcidin levels decreased to normal values in all patients. At baseline, a significant response of hepcidin to iron challenge was observed only in the subgroup with lower basal hepcidin concentration (P = 0.007). In iron-depleted patients, urinary hepcidin significantly increased after oral iron test (P = 0 .006). CONCLUSIONS: Ours findings suggest that in DIOS, the progression of iron accumulation is counteracted by the increase in hepcidin production and progressive reduction of iron absorption, explaining why these patients develop a mild-moderate iron overload that tends to a plateau. |
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Authors:
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Paola Trombini; Valentina Paolini; Sara Pelucchi; Raffaella Mariani; Elizabeta Nemeth; Tomas Ganz; Alberto Piperno |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't Date: 2011-04-18 |
Journal Detail:
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Title: Liver international : official journal of the International Association for the Study of the Liver Volume: 31 ISSN: 1478-3231 ISO Abbreviation: Liver Int. Publication Date: 2011 Aug |
Date Detail:
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Created Date: 2011-07-07 Completed Date: 2011-11-18 Revised Date: 2012-05-30 |
Medline Journal Info:
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Nlm Unique ID: 101160857 Medline TA: Liver Int Country: England |
Other Details:
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Languages: eng Pagination: 994-1000 Citation Subset: IM |
Copyright Information:
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© 2011 John Wiley & Sons A/S. |
Affiliation:
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Department of Clinical Medicine and Prevention, Centre for Diagnosis and Therapy of Hemochromatosis, S. Gerardo Hospital, University of Milano-Bicocca, Monza, Italy. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Administration, Oral Alanine Transaminase / blood Antimicrobial Cationic Peptides / metabolism*, urine Blood Glucose / analysis C-Reactive Protein / analysis Cholesterol / blood DNA Mutational Analysis Female Hemoglobins / analysis Histocompatibility Antigens Class I / genetics Humans Insulin / blood Iron / administration & dosage, metabolism* Iron Overload / metabolism*, physiopathology* Italy Liver / metabolism, pathology* Male Membrane Proteins / genetics Statistics, Nonparametric Triglycerides / blood gamma-Glutamyltransferase / blood |
| Grant Support | |
ID/Acronym/Agency:
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R01 DK082717/DK/NIDDK NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Antimicrobial Cationic Peptides; 0/Blood Glucose; 0/HFE protein, human; 0/Hemoglobins; 0/Histocompatibility Antigens Class I; 0/Insulin; 0/Membrane Proteins; 0/Triglycerides; 0/hepcidin; 57-88-5/Cholesterol; 7439-89-6/Iron; 9007-41-4/C-Reactive Protein; EC 2.3.2.2/gamma-Glutamyltransferase; EC 2.6.1.2/Alanine Transaminase |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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