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

    Access Status
    Open access via publisher
    Authors
    Newsholme, Philip
    Morgan, D.
    Rebelato, E.
    Oliveira-Emilio, H.
    Procopio, J.
    Curi, R.
    Carpinelli, A.
    Date
    2009
    Type
    Journal Article
    
    Metadata
    Show full item record
    Citation
    Newsholme, P. and Morgan, D. and Rebelato, E. and Oliveira-Emilio, H. and Procopio, J. and Curi, R. and Carpinelli, A. 2009. Insights into the critical role of NADPH oxidase(s) in the normal and dysregulated pancreatic beta cell. Diabetologia. 52 (12): pp. 2489-2498.
    Source Title
    Diabetologia
    DOI
    10.1007/s00125-009-1536-z
    ISSN
    0012-186X
    School
    School of Biomedical Sciences
    URI
    http://hdl.handle.net/20.500.11937/18782
    Collection
    • Curtin Research Publications
    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 H2O2 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. © 2009 Springer-Verlag.

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