The Role of Mitophagy in Diabetes
All forms of diabetes share the common etiology of insufficient insulin release from pancreatic islet beta cells to meet peripheral insulin demand. Beta cells require mitochondrial function in order to maintain proper glucose stimulated insulin release. Our lab focuses on the molecular and genetic regulation of the mitochondrial life cycle, with a focus on mitophagy, a pathway to dispose of unhealthy or damaged mitochondria. Our studies also focus on novel genetic targets affecting the mitophagy pathway, which are also associated with diabetes in humans through studies in cellular and mouse genetic model systems as well as isolated human islets. Our goal is discover how the dysregulation of mitochondrial respiration and mitophagy leads to diabetes pathogenesis as well as determining strategies to improve mitophagy to prevent or treat diabetes in humans.