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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...
Autores principales: | , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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Molecular Diversity Preservation International (MDPI)
2012
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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. |
format | Online Article Text |
id | pubmed-3497347 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2012 |
publisher | Molecular Diversity Preservation International (MDPI) |
record_format | MEDLINE/PubMed |
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 |
work_keys_str_mv | AT kanetohideaki involvementofoxidativestressinsuppressionofinsulinbiosynthesisunderdiabeticconditions AT matsuokatakaaki involvementofoxidativestressinsuppressionofinsulinbiosynthesisunderdiabeticconditions |