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Diabetologia. 2009 Dec;52(12):2489-98. doi: 10.1007/s00125-009-1536-z. Epub 2009 Oct 7.

Insights into the critical role of NADPH oxidase(s) in the normal and dysregulated pancreatic beta cell.

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  • 1UCD School of Biomolecular and Biomedical Science, UCD Conway Institute and Health Sciences Centre, UCD Dublin, Belfield, Dublin 4, Ireland. philip.newsholme@ucd.ie

Abstract

It is now widely accepted that reactive oxygen species (ROS) contribute to cell and tissue dysfunction and damage in diabetes. The source of ROS in the insulin secreting pancreatic beta cells has traditionally been considered to be the mitochondrial electron transport chain. While this source is undoubtedly important, we fully describe in this article recent information and evidence of NADPH oxidase-dependent generation of ROS in pancreatic beta cells and identify the various isoforms that contribute to O(2)(*-) and H(2)O(2) production in various conditions. While glucose-stimulated ROS generation may be important for acute regulation of insulin secretion, at higher levels ROS may disrupt mitochondrial energy metabolism. However, ROS may alter other cellular processes such as signal transduction, ion fluxes and/or cell proliferation/death. The various beta cell isoforms of NADPH oxidase (described in this review) may, via differences in the kinetics and species of ROS generated, positively and negatively regulate insulin secretion and cell survival.

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