Publications

Abstract

Insulin-producing pancreatic beta-cells are central to glucose homeostasis, and their failure is a principal driver of diabetes development. To preserve optimal health beta-cells must withstand both intrinsic and extrinsic stressors, ranging from inflammation to increased peripheral insulin demand, in addition to maintaining insulin biosynthesis and secretory machinery. Autophagy is increasingly being appreciated as a critical beta-cell quality control system vital for glycemic control. Here we focus on the underappreciated, yet crucial, roles for selective and organelle-specific forms of autophagy as mediators of beta-cell health. We examine the unique molecular players underlying each distinct form of autophagy in beta-cells, including selective autophagy of mitochondria, insulin granules, lipid, intracellular amyloid aggregates, endoplasmic reticulum, and peroxisomes. We also describe how defects in selective autophagy pathways contribute to the development of diabetes. As all forms of autophagy are not the same, a refined view of beta-cell selective autophagy may inform new approaches to defend against the various insults leading to beta-cell failure in diabetes.