PurposePancreatic beta-cells play a critical role in regulating plasma insulin levels and glucose metabolism balance, with their dysfunction being a key factor in the progression of diabetes. This review aims to explore the role of autophagy, a vital cellular self-maintenance process, in preserving pancreatic beta-cell functionality and its implications in diabetes pathogenesis.MethodsWe examine the current literature on the role of autophagy in beta-cells, highlighting its function in maintaining cell structure, quantity, and function. The review also discusses the effects of both excessive and insufficient autophagy on beta-cell dysfunction and glucose metabolism imbalance. Furthermore, we discuss potential therapeutic agents that modulate the autophagy pathway to influence beta-cell function, providing insights into therapeutic strategies for diabetes management.ResultsAutophagy acts as a self-protective mechanism within pancreatic beta-cells, clearing damaged organelles and proteins to maintain cellular stability. Abnormal autophagy activity, either overactive or deficient, can disrupt beta-cell function and glucose regulation, contributing to diabetes progression.ConclusionAutophagy plays a pivotal role in maintaining pancreatic beta-cell function, and its dysregulation is implicated in the development of diabetes. Targeting the autophagy pathway offers potential therapeutic strategies for diabetes management, with agents that modulate autophagy showing promise in preserving beta-cell function.