Please use this identifier to cite or link to this item: http://hdl.handle.net/10397/60137
Title: Hepcidin and iron homeostasis
Other Titles: Hepcidin和铁稳态
Authors: Chang, YZ
Yuan, QP
Zhou, B
Qian, ZM
Keywords: Hepcidin
Iron metabolism
Issue Date: 2003
Publisher: 中國學術期刊 (光盤版) 電子雜誌社
Source: 中华内分泌代谢杂志 (Chinese journal of endocrinology and metabolism), Dec. 2003, v. 19, no. 6, p. 501-504 How to cite?
Journal: 中华内分泌代谢杂志 (Chinese journal of endocrinology and metabolism) 
Abstract: 铁代谢紊乱引起的疾患是人类最常见的疾病。生理条件下 ,人体主要通过调控小肠铁吸收保持机体铁稳态。最近关于hepcidin的研究显示 ,这种肝脏合成的已知具有抗菌功能的多肽是控制小肠铁吸收 ,以及调节机体铁稳态的铁调节激素。肝脏hepcidin高表达可能是许多贫血包括炎症和慢性疾病性贫血的根本原因 ,而hepcidin表达障碍可能是许多铁过负荷类疾病的起因。
The understanding of iron metabolism in humans, especially of its mechanism involved in controlling iron absorption in the proximal small intestine, is of great importance since diseases associated with iron deficiency or overload are very common worldwide. Recent study on hepcidin which is senthesized by liver has showed that this originally identified as a circulating antimicrobial peptide is a putative iron regulatory hormone. It plays a central role in the regulation of small intestine iron absorption and body iron homeostasis. The increased expression of hepcidin in the liver, induced by inflammation, might be an initial cause of the anemia of infection or chronic diseases and the iron-overload diseases might be tightly associated with the decreased hepcidin expression in the liver.
URI: http://hdl.handle.net/10397/60137
ISSN: 1000-6699
Rights: © 2003 中国学术期刊电子杂志出版社。本内容的使用仅限于教育、科研之目的。
© 2003 China Academic Journal Electronic Publishing House. It is to be used strictly for educational and research purposes.
Appears in Collections:Journal/Magazine Article

Files in This Item:
File Description SizeFormat 
r17418.pdf158.97 kBAdobe PDFView/Open
Access
View full-text via PolyU eLinks SFX Query
Show full item record

Page view(s)

9
Last Week
3
Last month
Checked on May 21, 2017

Download(s)

9
Checked on May 21, 2017

Google ScholarTM

Check



Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.