Document Detail


Hepcidin response to acute iron intake and chronic iron loading in dysmetabolic iron overload syndrome.
MedLine Citation:
PMID:  21733088     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
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.
Authors:
Paola Trombini; Valentina Paolini; Sara Pelucchi; Raffaella Mariani; Elizabeta Nemeth; Tomas Ganz; Alberto Piperno
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2011-04-18
Journal Detail:
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:
Created Date:  2011-07-07     Completed Date:  2011-11-18     Revised Date:  2012-05-30    
Medline Journal Info:
Nlm Unique ID:  101160857     Medline TA:  Liver Int     Country:  England    
Other Details:
Languages:  eng     Pagination:  994-1000     Citation Subset:  IM    
Copyright Information:
© 2011 John Wiley & Sons A/S.
Affiliation:
Department of Clinical Medicine and Prevention, Centre for Diagnosis and Therapy of Hemochromatosis, S. Gerardo Hospital, University of Milano-Bicocca, Monza, Italy.
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MeSH Terms
Descriptor/Qualifier:
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:
R01 DK082717/DK/NIDDK NIH HHS
Chemical
Reg. No./Substance:
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

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