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Involvement of Oxidative Stress in Suppression of Insulin Biosynthesis under Diabetic Conditions

Type 2 diabetes is characterized by pancreatic β-cell dysfunction and insulin resistance, and the number of patients has markedly increased worldwide. In the diabetic state, hyperglycemia per se and subsequent induction of oxidative stress decrease insulin biosynthesis and secretion, leading to the...

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Detalles Bibliográficos
Autores principales: Kaneto, Hideaki, Matsuoka, Taka-aki
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Molecular Diversity Preservation International (MDPI) 2012
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3497347/
https://www.ncbi.nlm.nih.gov/pubmed/23202973
http://dx.doi.org/10.3390/ijms131013680
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author Kaneto, Hideaki
Matsuoka, Taka-aki
author_facet Kaneto, Hideaki
Matsuoka, Taka-aki
author_sort Kaneto, Hideaki
collection PubMed
description Type 2 diabetes is characterized by pancreatic β-cell dysfunction and insulin resistance, and the number of patients has markedly increased worldwide. In the diabetic state, hyperglycemia per se and subsequent induction of oxidative stress decrease insulin biosynthesis and secretion, leading to the aggravation of Type 2 diabetes. In addition, there is substantial reduction in expression and/or activities of several insulin gene transcription factors. This process is known as β-cell glucose toxicity, which is often observed under diabetic conditions. Taken together, it is likely that oxidative stress explains, at least in part, the molecular mechanism for β-cell glucose toxicity, which is often observed in Type 2 diabetes.
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spelling pubmed-34973472012-11-29 Involvement of Oxidative Stress in Suppression of Insulin Biosynthesis under Diabetic Conditions Kaneto, Hideaki Matsuoka, Taka-aki Int J Mol Sci Review Type 2 diabetes is characterized by pancreatic β-cell dysfunction and insulin resistance, and the number of patients has markedly increased worldwide. In the diabetic state, hyperglycemia per se and subsequent induction of oxidative stress decrease insulin biosynthesis and secretion, leading to the aggravation of Type 2 diabetes. In addition, there is substantial reduction in expression and/or activities of several insulin gene transcription factors. This process is known as β-cell glucose toxicity, which is often observed under diabetic conditions. Taken together, it is likely that oxidative stress explains, at least in part, the molecular mechanism for β-cell glucose toxicity, which is often observed in Type 2 diabetes. Molecular Diversity Preservation International (MDPI) 2012-10-22 /pmc/articles/PMC3497347/ /pubmed/23202973 http://dx.doi.org/10.3390/ijms131013680 Text en © 2012 by the authors; licensee Molecular Diversity Preservation International, Basel, Switzerland. http://creativecommons.org/licenses/by/3.0 This article is an open-access article distributed under the terms and conditions of the Creative Commons Attribution license (http://creativecommons.org/licenses/by/3.0).
spellingShingle Review
Kaneto, Hideaki
Matsuoka, Taka-aki
Involvement of Oxidative Stress in Suppression of Insulin Biosynthesis under Diabetic Conditions
title Involvement of Oxidative Stress in Suppression of Insulin Biosynthesis under Diabetic Conditions
title_full Involvement of Oxidative Stress in Suppression of Insulin Biosynthesis under Diabetic Conditions
title_fullStr Involvement of Oxidative Stress in Suppression of Insulin Biosynthesis under Diabetic Conditions
title_full_unstemmed Involvement of Oxidative Stress in Suppression of Insulin Biosynthesis under Diabetic Conditions
title_short Involvement of Oxidative Stress in Suppression of Insulin Biosynthesis under Diabetic Conditions
title_sort involvement of oxidative stress in suppression of insulin biosynthesis under diabetic conditions
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3497347/
https://www.ncbi.nlm.nih.gov/pubmed/23202973
http://dx.doi.org/10.3390/ijms131013680
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