Abstract
Failure of pancreatic β-cells is the common characteristic of type 1 and type 2 diabetes. Type 1 diabetes mellitus is induced by destruction of pancreatic β-cells which is mediated by an autoimmune mechanism and consequent inflammatory process. Various inflammatory cytokines and oxidative stress are produced during this process, which has been proposed to play an important role in mediating β-cell destruction. The JNK pathway is also activated by such cytokines and oxidative stress, and is involved in β-cell destruction. Type 2 diabetes is the most prevalent and serious metabolic disease, and β-cell dysfunction and insulin resistance are the hallmark of type 2 diabetes. Under diabetic conditions, chronic hyperglycemia gradually deteriorates β-cell function and aggravates insulin resistance. This process is called “glucose toxicity”. Under such conditions, oxidative stress is provoked and the JNK pathway is activated, which is likely involved in pancreatic β-cells dysfunction and insulin resistance. In addition, oxidative stress and activation of the JNK pathway are also involved in the progression of atherosclerosis which is often observed under diabetic conditions. Taken together, it is likely that oxidative stress and subsequent activation of the JNK pathway are involved in the pathogenesis of type 1 and type 2 diabetes.
Keywords: Oxidative stress, the JNK pathway, type 1 diabetes, type 2 diabetes, β-cell glucose toxicity, insulin resistance, atherosclerosis
Current Molecular Medicine
Title: Oxidative Stress and the JNK Pathway are Involved in the Development of Type 1 and Type 2 Diabetes
Volume: 7 Issue: 7
Author(s): Hideaki Kaneto, Taka-aki Matsuoka, Naoto Katakami, Dan Kawamori, Takeshi Miyatsuka, Kazutomi Yoshiuchi, Tetsuyuki Yasuda, Ken'ya Sakamoto, Yoshimitsu Yamasaki and Munehide Matsuhisa
Affiliation:
Keywords: Oxidative stress, the JNK pathway, type 1 diabetes, type 2 diabetes, β-cell glucose toxicity, insulin resistance, atherosclerosis
Abstract: Failure of pancreatic β-cells is the common characteristic of type 1 and type 2 diabetes. Type 1 diabetes mellitus is induced by destruction of pancreatic β-cells which is mediated by an autoimmune mechanism and consequent inflammatory process. Various inflammatory cytokines and oxidative stress are produced during this process, which has been proposed to play an important role in mediating β-cell destruction. The JNK pathway is also activated by such cytokines and oxidative stress, and is involved in β-cell destruction. Type 2 diabetes is the most prevalent and serious metabolic disease, and β-cell dysfunction and insulin resistance are the hallmark of type 2 diabetes. Under diabetic conditions, chronic hyperglycemia gradually deteriorates β-cell function and aggravates insulin resistance. This process is called “glucose toxicity”. Under such conditions, oxidative stress is provoked and the JNK pathway is activated, which is likely involved in pancreatic β-cells dysfunction and insulin resistance. In addition, oxidative stress and activation of the JNK pathway are also involved in the progression of atherosclerosis which is often observed under diabetic conditions. Taken together, it is likely that oxidative stress and subsequent activation of the JNK pathway are involved in the pathogenesis of type 1 and type 2 diabetes.
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Kaneto Hideaki, Matsuoka Taka-aki, Katakami Naoto, Kawamori Dan, Miyatsuka Takeshi, Yoshiuchi Kazutomi, Yasuda Tetsuyuki, Sakamoto Ken'ya, Yamasaki Yoshimitsu and Matsuhisa Munehide, Oxidative Stress and the JNK Pathway are Involved in the Development of Type 1 and Type 2 Diabetes, Current Molecular Medicine 2007; 7 (7) . https://dx.doi.org/10.2174/156652407782564408
DOI https://dx.doi.org/10.2174/156652407782564408 |
Print ISSN 1566-5240 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-5666 |
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