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    Molecular mechanisms of ROS production and oxidative stress in diabetes

    Access Status
    Fulltext not available
    Authors
    Newsholme, Philip
    Cruzat, Vinicius
    Keane, Kevin
    Carlessi, Rodrigo
    de Bittencourt, P.
    Date
    2016
    Type
    Journal Article
    
    Metadata
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    Citation
    Newsholme, P. and Cruzat, V. and Keane, K. and Carlessi, R. and de Bittencourt, P. 2016. Molecular mechanisms of ROS production and oxidative stress in diabetes. Biochemical Journal. 473 (24): pp. 4527-4550.
    Source Title
    Biochemical Journal
    DOI
    10.1042/BCJ20160503C
    School
    School of Biomedical Sciences
    URI
    http://hdl.handle.net/20.500.11937/11782
    Collection
    • Curtin Research Publications
    Abstract

    Oxidative stress and chronic inflammation are known to be associated with the development of metabolic diseases, including diabetes. Oxidative stress, an imbalance between oxidative and antioxidative systems of cells and tissues, is a result of over production of oxidative-free radicals and associated reactive oxygen species (ROS). One outcome of excessive levels of ROS is the modification of the structure and function of cellular proteins and lipids, leading to cellular dysfunction including impaired energy metabolism, altered cell signalling and cell cycle control, impaired cell transport mechanisms and overall dysfunctional biological activity, immune activation and inflammation. Nutritional stress, such as that caused by excess high-fat and/or carbohydrate diets, promotes oxidative stress as evident by increased lipid peroxidation products, protein carbonylation and decreased antioxidant status. In obesity, chronic oxidative stress and associated inflammation are the underlying factors that lead to the development of pathologies such as insulin resistance, dysregulated pathways of metabolism, diabetes and cardiovascular disease through impaired signalling and metabolism resulting in dysfunction to insulin secretion, insulin action and immune responses. However, exercise may counter excessive levels of oxidative stress and thus improve metabolic and inflammatory outcomes. In the present article, we review the cellular and molecular origins and significance of ROS production, the molecular targets and responses describing how oxidative stress affects cell function including mechanisms of insulin secretion and action, from the point of view of possible application of novel diabetic therapies based on redox regulation.

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