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题名:Iron: the hard player in diabetes pathophysiology.
作者:HANSEN JB; MOEN IW; MANDRUP-POULSEN T;
来源:Acta Physiol (Oxf). 2014 Feb 12. doi: 10.1111/apha.12256. [ IF= 0.00 ] ]
URL :10.1111/apha.12256
日期:20140317
摘要:The interest in the role of ferrous iron in diabetes pathophysiology has been
revived by recent evidence of iron as an important determinant of pancreatic
islet inflammation and as a biomarker of diabetes risk and mortality. The iron
metabolism in the beta-cell is complex. Excess free iron is toxic, but at the
same time iron is required for normal beta-cell function and thereby glucose
homeostasis. In the pathogenesis of diabetes, iron generates reactive oxygen
species (ROS) by participating in the Fenton chemistry, which can induce
oxidative damage and apoptosis. The aim of this review is to present and discuss
recent evidence suggesting that iron is a key pathogenic factor in both type 1
and type 2 diabetes with a focus on inflammatory pathways. Pro-inflammatory
cytokine-induced beta-cell death is not fully understood, but may include iron
induced ROS formation resulting in de-differentiation by activation of
transcription factors, activation of the mitochondrial apoptotic machinery or of
other cell-death mechanisms. The pro-inflammatory cytokine IL-1beta facilitates
divalent metal transporter 1 (DMT1) induced beta-cell iron-uptake and
consequently ROS-formation and apoptosis, and we propose that this mechanism
provides the relay between inflammation and oxidative beta-cell damage. Iron
chelation may be a potential therapeutic approach to reduce disease severity and
mortality among diabetes patients. However, the therapeutic effect and safety of
iron reduction needs to be tested in clinical trials before dietary interventions
of the use of titrated iron chelation therapy to avoid anaemia. This article is
protected by copyright. All rights reserved.

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