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Transfer of reducing equivalents between cytosolic compartments and the mitochondrial matrix is mediated by NADH shuttles. Among these, the malate–aspartate shuttle has been proposed to play a major role in β-cells for the control of glucose-stimulated insulin secretion. AGC1 or Aralar1 (aspartate–glutamate carrier 1) is a key component of the malate–aspartate shuttle. Overexpression of AGC1 increases the capacity of the malate–aspartate shuttle, resulting in enhanced metabolism–secretion coupling, both in INS-1E cells and rat islets. In the present study, knockdown of AGC1 was achieved in the same β-cell models, using adenovirus-mediated delivery of shRNA (small-hairpin RNA). Compared with control INS-1E cells, down-regulation of AGC1 blunted NADH formation (−57%; P |
