Hepcidin, the principal iron regulatory hormone, regulates the absorption of iron from the diet and the mobilization of iron from stores. Previous studies indicated that hepcidin is suppressed during anemia, a response that would appropriately increase the absorption of iron and its release from stores. Indeed, in the mouse model, hepcidin-1 was suppressed after phlebotomy or erythropoietin administration but the suppression was reversed by inhibitors of erythropoiesis. The suppression of hepcidin necessary to match iron supply to erythropoietic demand thus requires increased erythropoiesis and is not directly mediated by anemia, tissue hypoxia, or erythropoietin.
Suppression of hepcidin during anemia requires erythropoietic activity. Publishing Authors By Initials
Suppression of hepcidin during anemia requires erythropoietic activity. Journal Published:
PUBLICATION TYPE: Research Support, Non-U.S. Gov
Journal: Blood
VOLUME: 108
Page Numbers: 3730-5
Journal Abbreviation: Blood
ISSN: 0006-4971
DAY: 1
MONTH: 08
YEAR: 2006
Suppression of hepcidin during anemia requires erythropoietic activity. Information
Number of References:
LANGUAGE: eng
NlmUniqueID: 7603509
Suppression of hepcidin during anemia requires erythropoietic activity. Keywords Mesh Terms:
KEYWORDS: Mice
MESH TERMS: metabolism
Chemical & Substance for Abstract: Suppression of hepcidin during anemia requires erythropoietic activity. Information
Substance Name: Iron
Registry Number: 7439-89-6
Grant and Affiliation Information for Suppression of hepcidin during anemia requires erythropoietic activity.
AFFILIATION: Division of Pulmonary and Critical Care Medicine, David Geffen School of Medicine at the University of California (UCLA), Los Angeles, USA.
Country: United States
AGENCY: United States NIDDK
GRANT: R01 DK 065029
ACRONYM: DK
MEDLINETA: Blood
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DATABASENAME:
ACCESSION NUMBER:
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