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    Reactive oxygen and nitrogen species generation, antioxidant defenses, and β-cell function: a critical role for amino acids

    Access Status
    Open access via publisher
    Authors
    Newsholme, Philip
    Rebelato, E.
    Abdulkader, F.
    Krause, M.
    Carpinelli, A.
    Curi, R.
    Date
    2012
    Type
    Journal Article
    
    Metadata
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    Citation
    Newsholme, P. and Rebelato, E. and Abdulkader, F. and Krause, M. and Carpinelli, A. and Curi, R. 2012. Reactive oxygen and nitrogen species generation, antioxidant defenses, and β-cell function: a critical role for amino acids. Journal of Endocrinology. 214: pp. 11-20.
    Source Title
    Journal of Endocrinology
    DOI
    10.1530/JOE-12-0072
    ISSN
    0022-0795
    URI
    http://hdl.handle.net/20.500.11937/26446
    Collection
    • Curtin Research Publications
    Abstract

    Growing evidence indicates that the regulation of intracellular reactive oxygen species (ROS) and reactive nitrogen species (RNS) levels is essential for maintaining normal β-cell glucose responsiveness. While long-term exposure to high glucose induces oxidative stress in β cells, conflicting results have been published regarding the impact of ROS on acute glucose exposure and their role in glucose stimulated insulin secretion (GSIS). Although β cells are considered to be particularly vulnerable to oxidative damage, as they express relatively low levels of some peroxide-metabolizing enzymes such as catalase and glutathione (GSH) peroxidase, other less known GSH-based antioxidant systems are expressed in β cells at higher levels. Herein, we discuss the key mechanisms of ROS/RNS production and their physiological function in pancreatic β cells. We also hypothesize that specific interactions between RNS and ROS may be the cause of the vulnerability of pancreatic β cells to oxidative damage. In addition, using a hypothetical metabolic model based on the data available in the literature, we emphasize the importance of amino acid availability for GSH synthesis and for the maintenance of β-cell function and viability during periods of metabolic disturbance before the clinical onset of diabetes.

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