Figure 1.

The effect of mitoNEET induction on mass and function of pancreatic islets. The oxidation of glucose in β-cells via mitochondria produces ATP, which closes ATP-dependent potassium channels. This causes β-cell depolarization and calcium influx, which triggers insulin secretion. Factors released from β-cells contribute to glucose-mediated suppression of α-cell function. Induction of mitoNEET in β-cells, α-cells, or both have different impacts on β-cell mass and function, resulting in different in vivo phenotypes that partially—but not completely—resemble the conditions in type 2 diabetes.