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Title

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

Authors
Bender, Katrin
McClenaghan, Neville H.
Flatt, Peter R.
Newsholme, Philip
Published in Clinical Science. 2009, vol. 117, no. 9, p. 321-330
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 beta-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.
Keywords Adenoviridae/geneticsAlanine/metabolism/pharmacologyAnimalsCell LineGenetic VectorsGlucose/pharmacologyGlutamine/metabolismGlycogen/metabolismInsulin/*metabolismInsulin-Secreting Cells/drug effects/*metabolismMembrane Transport Proteins/*metabolism/physiologyMitochondrial Membrane Transport ProteinsMitochondrial Proteins/*metabolism/physiologyRatsTransduction, GeneticTriglycerides/metabolism
Identifiers
PMID: 19344310
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Structures
Research group Mitochondries et sécrétion d'insuline (671)
Citation
(ISO format)
BENDER, Katrin et al. Overexpression of the malate-aspartate NADH shuttle member Aralar1 in the clonal beta-cell line BRIN-BD11 enhances amino-acid-stimulated insulin secretion and cell metabolism. In: Clinical Science, 2009, vol. 117, n° 9, p. 321-330. https://archive-ouverte.unige.ch/unige:19671

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Deposited on : 2012-04-23

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