Elucidating the molecular mechanism of autophagy was a landmark in understanding not only the physiology of cells and tissues, but also the pathogenesis of diverse diseases, including diabetes and metabolic disorders. Autophagy of pancreatic β‐cells plays a pivotal role in the maintenance of the mass, structure and function of β‐cells, whose dysregulation can lead to abnormal metabolic profiles or diabetes. Modulators of autophagy are being developed to improve metabolic profile and β‐cell function through the removal of harmful materials and rejuvenation of organelles, such as mitochondria and endoplasmic reticulum. Among the known antidiabetic drugs, glucagon‐like peptide‐1 receptor agonists enhance the autophagic activity of β‐cells, which might contribute to the profound effects of glucagon‐like peptide‐1 receptor agonists on systemic metabolism. In this review, the results from studies on the role of autophagy in β‐cells and their implication in the development of diabetes are discussed. In addition to non‐selective (macro)autophagy, the role and mechanisms of selective autophagy and other minor forms of autophagy that might occur in β‐cells are discussed. As β‐cell failure is the ultimate cause of diabetes and unresponsiveness to conventional therapy, modulation of β‐cell autophagy might represent a future antidiabetic treatment approach, particularly in patients who are not well managed with current antidiabetic therapy.

中文翻译：

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β细胞自噬在β细胞生理学和糖尿病发生中的作用

阐明自噬的分子机制不仅对于理解细胞和组织的生理学，而且对于理解包括糖尿病和代谢紊乱在内的多种疾病的发病机制具有里程碑意义。胰腺β细胞的自噬在维持β细胞的质量、结构和功能中发挥着关键作用，β细胞的失调可导致代谢特征异常或糖尿病。人们正在开发自噬调节剂，通过去除有害物质和恢复线粒体和内质网等细胞器的活力来改善代谢状况和 β 细胞功能。在已知的抗糖尿病药物中，胰高血糖素样肽-1受体激动剂可增强β细胞的自噬活性，这可能有助于胰高血糖素样肽-1受体激动剂对全身代谢的深远影响。在这篇综述中，讨论了自噬在 β 细胞中的作用及其在糖尿病发展中的意义的研究结果。除了非选择性（宏观）自噬之外，还讨论了 β 细胞中可能发生的选择性自噬和其他次要形式的自噬的作用和机制。由于 β 细胞衰竭是糖尿病和对常规治疗无反应的最终原因，因此调节 β 细胞自噬可能代表未来的抗糖尿病治疗方法，特别是对于当前抗糖尿病治疗效果不佳的患者。