Abstract
Zhang et al. recently proposed a new mechanism of metabolism-secretion coupling impairment in diabetic β-cells involving the loss of cytosolic adenosine triphosphate by leakage through plasma membrane. Hyperglycemia increases mistargeting expression of the adenosine triphosphate-conducting mitochondrial outer membrane voltage-dependent anion channel-1 on the plasma membrane leading to adenosine triphosphate depletion. The interaction between reactive oxygen species overproduction and voltage-dependent anion channel-1 induction is an interesting issue to be resolved.