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Scientific article
English

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

Published inClinical science, vol. 117, no. 9, p. 321-330
Publication date2009
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/genetics
  • Alanine/metabolism/pharmacology
  • Animals
  • Cell Line
  • Genetic Vectors
  • Glucose/pharmacology
  • Glutamine/metabolism
  • Glycogen/metabolism
  • Insulin/*metabolism
  • Insulin-Secreting Cells/drug effects/*metabolism
  • Membrane Transport Proteins/*metabolism/physiology
  • Mitochondrial Membrane Transport Proteins
  • Mitochondrial Proteins/*metabolism/physiology
  • Rats
  • Transduction, Genetic
  • Triglycerides/metabolism
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. doi: 10.1042/CS20090126
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ISSN of the journal0143-5221
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