The BECN1-BCL2 complex regulates insulin secretion and storage in mice.

Macroautophagy/autophagy abnormality has been recently associated with metabolic disorders, such as type 2 diabetes (T2D). However, the effect of autophagy activation in systemic energy metabolism was poorly understood. In our recent study, we demonstrated that autophagy plays different roles in distinct metabolic tissues, using an autophagy-hyperactive mouse model. In insulin-producing β cells, excess autophagy degrades insulin-containing vesicles (a process termed vesicophagy), resulting in decreased insulin contents and systemic glucose intolerance; whereas in insulin-responsive cells, activating autophagy decreases endoplasmic reticulum (ER) stress and improves insulin sensitivity.