In the beta cell, mitochondrial Redox- NADH- shuttles are important for coupling glycolysis to mitochondrial energy metabolism. Aralar1, a mitochondrial Aspartate-Glutamate exchanger in the Malate-Aspartate shuttle, has been found to be important for regulation of insulin secretion and glucose metabolism in the INS- 1E cell line as well as in the clonal BRIN- BD11 cell line. Certain amino acids, in particular L- alanine, L-Leucine and L- glutamine, are known to stimulate insulin secretion and glucose metabolism in primary islets and cell lines including BRIN- BD11 either on their own or synergistically in combination with glucose. We have now over- expressed Aralar1 by the means of the recombinant Adenovirus AdCA- Aralar1 and have subsequently investigated the impact of Aralar1 on insulin secretion and metabolism, using glucose, pyruvate and various amino acids as fuel stimuli. We have also investigated the effects of an inhibitor of aminotransferase reactions, important for amino acid metabolism (Aminooxyaxctetate), and a calcium chelator (BAPTA-AM). Experimental parameters measured were insulin secretion, glucose and glutamine consumption, lactate and glutamate generation, mitochondrial membrane potential, NADH generation, triglyceride and glycogen content. Generally, Aralar1 over- expression in BRIN-BD11 cells resulted in a potentiation of insulin secretion, glucose consumption, mitochondrial membrane hyperpolarization and NADH generation (p<0.05 for all parameters). All the latter effects were further enhanced by the presence of 10 mM L- alanine. However, insulin secretion and glucose consumption were reduced by the presence of 10mM L- aspartate. Addition of L- glutamine did not have a significant impact on any of the latter parameters.