Authors: Kaneto, Hideaki; Matsuoka, Taka-aki; Katakami, Naoto; Kawamori, Dan; Miyatsuka, Takeshi; Yoshiuchi, Kazutomi; Yasuda, Tetsuyuki; Sakamoto, Ken'ya; Yamasaki, Yoshimitsu; Matsuhisa, Munehide

Source: Current Molecular Medicine, Volume 7, Number 7, November 2007 , pp. 674-686(13)

Publisher: Bentham Science Publishers

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

Document Type: Research article

DOI: http://dx.doi.org/10.2174/156652407782564408

Publication date: 2007-11-01

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• Current Molecular Medicine is an interdisciplinary journal focused on providing the readership with current and comprehensive reviews on fundamental molecular mechanisms of disease pathogenesis, the development of molecular-diagnosis and/or novel approaches to rational treatment. The reviews should be of significant interest to basic researchers and clinical investigators in molecular medicine. Periodically the journal will invite guest editors to devote an issue on a basic research area that shows promise to advance our understanding of the molecular mechanism(s) of a disease or has potential for clinical applications.

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