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    L-glutamine supplementations enhance liver glutamine-glutathione axis and heat shock factor-1 expression in endurance-exercise trained rats

    Access Status
    Fulltext not available
    Authors
    Petry, E.
    Cruzat, Vinicius
    Heck, T.
    De Bittencourt, P.
    Tirapegui, J.
    Date
    2015
    Type
    Journal Article
    
    Metadata
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    Citation
    Petry, E. and Cruzat, V. and Heck, T. and De Bittencourt, P. and Tirapegui, J. 2015. L-glutamine supplementations enhance liver glutamine-glutathione axis and heat shock factor-1 expression in endurance-exercise trained rats. International Journal of Sport Nutrition and Exercise Metabolism. 25 (2): pp. 188-197.
    Source Title
    International Journal of Sport Nutrition and Exercise Metabolism
    DOI
    10.1123/ijsnem.2014-0131
    ISSN
    1526-484X
    School
    School of Biomedical Sciences
    URI
    http://hdl.handle.net/20.500.11937/40594
    Collection
    • Curtin Research Publications
    Abstract

    Liver L-glutamine is an important vehicle for the transport of ammonia and intermediary metabolism of amino acids between tissues, particularly under catabolic situations, such as high-intensity exercise. Hence, the aim of this study was to investigate the effects of oral supplementations with L-glutamine in its free or dipeptide forms (with L-alanine) on liver glutamine-glutathione (GSH) axis, and 70 kDa heat shock proteins (HSP70)/heat shock transcription factor 1 (HSF1) expressions. Adult male Wistar rats were 8-week trained (60 min/day, 5 days/week) on a treadmill. During the last 21 days, the animals were daily supplemented with 1 g of L-glutamine/kg body weight per day in either l-alanyl-L-glutamine dipeptide (DIP) form or a solution containing L-glutamine and l-alanine in their free forms (GLN+ALA) or water (controls). Exercise training increased cytosolic and nuclear HSF1 and HSP70 expression, as compared with sedentary animals. However, both DIP and GLN+ALA supplements enhanced HSF1 expression (in both cytosolic and nuclear fractions) in relation to exercised controls. Interestingly, HSF1 rises were not followed by enhanced HSP70 expression. DIP and GLN+ALA supplements increased plasma glutamine concentrations (by 62% and 59%, respectively) and glutamine to glutamate plasma ratio in relation to trained controls. This was in parallel with a decrease in plasma ammonium levels. Supplementations increased liver GSH (by 90%), attenuating the glutathione disulfide (GSSG) to GSH ratio, suggesting a redox state protection. In conclusion, oral administration with DIP and GLN+ALA supplements in endurance-trained rats improve liver glutamine-GSH axis and modulate HSF1 pathway.

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