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Int. J. Mol. Sci. 2012, 13(10), 13680-13690; doi:10.3390/ijms131013680

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

Department of Metabolic Medicine, Osaka University Graduate School of Medicine, 2-2 Yamadaoka, Suita, Osaka 565-0871, Japan
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Received: 11 September 2012 / Revised: 9 October 2012 / Accepted: 18 October 2012 / Published: 22 October 2012
(This article belongs to the Section Molecular Toxicology)
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Abstract

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.
Keywords: type 2 diabetes; pancreatic β-cells; glucose toxicity type 2 diabetes; pancreatic β-cells; glucose toxicity
This is an open access article distributed under the Creative Commons Attribution License (CC BY 3.0).

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MDPI and ACS Style

Kaneto, H.; Matsuoka, T.-A. Involvement of Oxidative Stress in Suppression of Insulin Biosynthesis under Diabetic Conditions. Int. J. Mol. Sci. 2012, 13, 13680-13690.

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