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Role of Reactive Oxygen Species in the Progression of Type 2 Diabetes and Atherosclerosis
Type 2 diabetes is the most prevalent and serious metabolic disease all over the world, and its hallmarks are pancreatic β-cell dysfunction and insulin resistance. Under diabetic conditions, chronic hyperglycemia and subsequent augmentation of reactive oxygen species (ROS) deteriorate β-cell functio...
Autores principales: | , , , |
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Formato: | Texto |
Lenguaje: | English |
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Hindawi Publishing Corporation
2010
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2825658/ https://www.ncbi.nlm.nih.gov/pubmed/20182627 http://dx.doi.org/10.1155/2010/453892 |
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author | Kaneto, Hideaki Katakami, Naoto Matsuhisa, Munehide Matsuoka, Taka-aki |
author_facet | Kaneto, Hideaki Katakami, Naoto Matsuhisa, Munehide Matsuoka, Taka-aki |
author_sort | Kaneto, Hideaki |
collection | PubMed |
description | Type 2 diabetes is the most prevalent and serious metabolic disease all over the world, and its hallmarks are pancreatic β-cell dysfunction and insulin resistance. Under diabetic conditions, chronic hyperglycemia and subsequent augmentation of reactive oxygen species (ROS) deteriorate β-cell function and increase insulin resistance which leads to the aggravation of type 2 diabetes. In addition, chronic hyperglycemia and ROS are also involved in the development of atherosclerosis which is often observed under diabetic conditions. Taken together, it is likely that ROS play an important role in the development of type 2 diabetes and atherosclerosis. |
format | Text |
id | pubmed-2825658 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2010 |
publisher | Hindawi Publishing Corporation |
record_format | MEDLINE/PubMed |
spelling | pubmed-28256582010-02-24 Role of Reactive Oxygen Species in the Progression of Type 2 Diabetes and Atherosclerosis Kaneto, Hideaki Katakami, Naoto Matsuhisa, Munehide Matsuoka, Taka-aki Mediators Inflamm Review Article Type 2 diabetes is the most prevalent and serious metabolic disease all over the world, and its hallmarks are pancreatic β-cell dysfunction and insulin resistance. Under diabetic conditions, chronic hyperglycemia and subsequent augmentation of reactive oxygen species (ROS) deteriorate β-cell function and increase insulin resistance which leads to the aggravation of type 2 diabetes. In addition, chronic hyperglycemia and ROS are also involved in the development of atherosclerosis which is often observed under diabetic conditions. Taken together, it is likely that ROS play an important role in the development of type 2 diabetes and atherosclerosis. Hindawi Publishing Corporation 2010 2010-02-16 /pmc/articles/PMC2825658/ /pubmed/20182627 http://dx.doi.org/10.1155/2010/453892 Text en Copyright © 2010 Hideaki Kaneto et al. https://creativecommons.org/licenses/by/3.0/ This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Review Article Kaneto, Hideaki Katakami, Naoto Matsuhisa, Munehide Matsuoka, Taka-aki Role of Reactive Oxygen Species in the Progression of Type 2 Diabetes and Atherosclerosis |
title | Role of Reactive Oxygen Species in the Progression of Type 2 Diabetes and Atherosclerosis |
title_full | Role of Reactive Oxygen Species in the Progression of Type 2 Diabetes and Atherosclerosis |
title_fullStr | Role of Reactive Oxygen Species in the Progression of Type 2 Diabetes and Atherosclerosis |
title_full_unstemmed | Role of Reactive Oxygen Species in the Progression of Type 2 Diabetes and Atherosclerosis |
title_short | Role of Reactive Oxygen Species in the Progression of Type 2 Diabetes and Atherosclerosis |
title_sort | role of reactive oxygen species in the progression of type 2 diabetes and atherosclerosis |
topic | Review Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2825658/ https://www.ncbi.nlm.nih.gov/pubmed/20182627 http://dx.doi.org/10.1155/2010/453892 |
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