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- W2152102707 startingPage "2348" @default.
- W2152102707 abstract "Emerging scientific evidence has disclosed unsuspected influences between iron metabolism and type 2 diabetes. The relationship is bi-directional--iron affects glucose metabolism, and glucose metabolism impinges on several iron metabolic pathways. Oxidative stress and inflammatory cytokines influence these relationships, amplifying and potentiating the initiated events. The clinical impact of these interactions depends on both the genetic predisposition and the time frame in which this network of closely related signals acts. In recent years, increased iron stores have been found to predict the development of type 2 diabetes while iron depletion was protective. Iron-induced damage might also modulate the development of chronic diabetes complications. Iron depletion has been demonstrated to be beneficial in coronary artery responses, endothelial dysfunction, insulin secretion, insulin action, and metabolic control in type 2 diabetes. Here, we show that iron modulates insulin action in healthy individuals and in patients with type 2 diabetes. The extent of this influence should be tested in large-scale clinical trials, searching for the usefulness and cost-effectiveness of therapeutic measures that decrease iron toxicity. The study of individual susceptibility and of the mechanisms that influence tissue iron deposition and damage are proposed to be valuable in anticipating and treating diabetes complications." @default.
- W2152102707 created "2016-06-24" @default.
- W2152102707 creator A5000296743 @default.
- W2152102707 creator A5007880285 @default.
- W2152102707 creator A5017184853 @default.
- W2152102707 date "2002-08-01" @default.
- W2152102707 modified "2023-10-14" @default.
- W2152102707 title "Cross-Talk Between Iron Metabolism and Diabetes" @default.
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- W2152102707 doi "https://doi.org/10.2337/diabetes.51.8.2348" @default.
- W2152102707 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/12145144" @default.
- W2152102707 hasPublicationYear "2002" @default.
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