Background: Metformin is widely believed to inhibit mitochondrial respiration. Results: Metformin increased phosphocreatine recovery from dinitrophenol or azide in intact cells, increased MTT reduction, left ATP levels unchanged, and increased free AMP. Conclusion: Metformin stimulated mitochondrial energy production. Significance: Distinct mechanisms for metformin other than mitochondrial inhibition, such as the inhibition of breakdown of AMP proposed in our work, need to be pursued.