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First published online on June 21, 2007.
 Copyright © 2007 by The Physiological Society
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Received May 4, 2007
Revised May 29, 2007
Accepted after revision June 19, 2007

Diabetes associated cell stress and dysfunction - Role of mitochondrial and non-mitochondrial ROS production and activity

Philip Newsholme1*, Ester Haber2, Sandro Hirabara3, Eduardo Rebelato3, Jochim Propcopio3, Daniela Morgan3, Henriette Oliveira-Emilio3, Angelo Carpinelli3, and Rui Curi3

1 UCD Dublin
2 Hebrew University Medical Centre Jerusalem
3 Department of Physiology and Biophysics, University of Sao Paulo

* To whom correspondence should be addressed. E-mail: philip.newsholme{at}ucd.ie.

It is now widely accepted, given the current weight of experimental evidence, that reactive oxygen species (ROS) contribute to cell and tissue dysfunction and damage caused by glucolipotoxicity in diabetes. The source of ROS in the insulin secreting pancreatic beta cells and in the cells which are targets for insulin action has been considered to be the mitochondrial electron transport chain. While this source is undoubtably important, we provide additional information and evidence for NADPH oxidase dependent generation of ROS both in pancreatic beta cells and in insulin sensitive cells. While mitochondrial ROS generation may be important for regulation of mitochondrial UCP activity and thus disruption of cellular energy metabolism, the NADPH oxidase associated ROS may alter parameters of signal transduction, insulin secretion, insulin action and cell proliferation or cell death. Thus NADPH oxidase may be a useful target for intervention strategies based on reversing the negative impact of glucolipotoxicity in diabetes.


Key words: Diabetes mellitus • Oxidative stress • Beta-cell




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