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ID 113753
Author
Tajima, Soichiro The University of Tokushima|Kyushu University
Enomoto, Hideaki The University of Tokushima
Imao, Mizuki The University of Tokushima
Horinouchi, Yuya The University of Tokushima
Kihira, Yoshitaka The University of Tokushima KAKEN Search Researchers
Miyamoto, Licht The University of Tokushima KAKEN Search Researchers
Keywords
Iron metabolism
Angiotensin II
Hepcidin
Ferritin
Content Type
Journal Article
Description
Purpose: Angiotensin II (ANG II) has been shown to affect iron metabolism through alteration of iron transporters, leading to increased cellular and tissue iron contents. Serum ferritin, a marker of body iron storage, is elevated in various cardiovascular diseases, including hypertension. However, the associated changes in iron absorption and the mechanism underlying increased iron content in a hypertensive state remain unclear.
Methods: C57BL6/J mice were treated with ANG II to generate a model of hypertension. Mice were divided into 3 groups: (1) control, (2) ANG II-treated, and (3) ANG II-treated and ANG II receptor blocker (ARB)-administered (ANG II-ARB) groups.
Results: Mice treated with ANG II showed increased serum ferritin levels compared to vehicle-treated control mice. In ANG II-treated mice, duodenal divalent metal transporter-1 (DMT1) and ferroportin (FPN) expression levels were increased and hepatic hepcidin mRNA expression and serum hepcidin concentration were reduced. The mRNA expression of bone morphogenetic protein 6 (BMP6) and CCAAT/enhancer binding protein alpha (C/EBPα), which are regulators of hepcidin, was also down-regulated in the livers of ANG II-treated mice. In terms of tissue iron content, macrophage iron content and renal iron content were increased by ANG II treatment, and these increases were associated with reduced expression of transferrin receptor 1 and FPN and increased expression of ferritin. These changes induced by ANG II treatment were ameliorated by administration of an ARB.
Conclusions: ANG II altered the expression of duodenal iron transporters and reduced hepcidin levels, contributing to the alteration of body iron distribution.
Journal Title
European Journal of Nutrition
ISSN
14366207
14366215
NCID
AA11323696
AA11622700
Publisher
Springer Berlin Heidelberg
Volume
54
Issue
5
Start Page
709
End Page
719
Published Date
2014-08-07
Remark
The final publication is available at link.springer.com.
EDB ID
DOI (Published Version)
URL ( Publisher's Version )
FullText File
language
eng
TextVersion
Author
departments
Medical Sciences
Pharmaceutical Sciences
University Hospital