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    Overexpression of the malate-aspartate NADH shuttle member Aralar1 in the clonal ß-cell line BRIN-BD11 enhances amino-acid-stimulated insulin secretion and cell metabolism

    Access Status
    Open access via publisher
    Authors
    Bender, K.
    Maechler, P.
    McClenaghan, N.
    Flatt, P.
    Newsholme, Philip
    Date
    2009
    Type
    Journal Article
    
    Metadata
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    Citation
    Bender, K. and Maechler, P. and McClenaghan, N. and Flatt, P. and Newsholme, P. 2009. Overexpression of the malate-aspartate NADH shuttle member Aralar1 in the clonal ß-cell line BRIN-BD11 enhances amino-acid-stimulated insulin secretion and cell metabolism. Clinical science (London, England : 1979). 117 (9): pp. 321-330.
    Source Title
    Clinical science (London, England : 1979)
    DOI
    10.1042/CS20090126
    ISSN
    0143-5221
    School
    School of Biomedical Sciences
    URI
    http://hdl.handle.net/20.500.11937/26084
    Collection
    • Curtin Research Publications
    Abstract

    In the present study, we have investigated the effects of the transduction with recombinant adenovirus AdCA-Aralar1 (aspartate-glutamate carrier 1) on the metabolism, function and secretory properties of the glucose- and amino-acid-responsive clonal insulin-secreting cell line BRIN-BD11. Aralar1 overexpression increased long-term (24 h) and acute (20 min) glucose- and amino-acid-stimulated insulin secretion, cellular glucose metabolism, L-alanine and L-glutamine consumption, cellular ATP and glutamate concentrations, and stimulated glutamate release. However, cellular triacylglycerol and glycogen contents were decreased as was lactate production. These findings indicate that increased malate-aspartate shuttle activity positively shifted ß-cell metabolism, thereby increasing glycolysis capacity, stimulus-secretion coupling and, ultimately, enhancing insulin secretion. We conclude that Aralar1 is a key metabolic control site in insulin-secreting cells.

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