BACKGROUND Elucidation of the basic molecular mechanism of autophagy was a breakthrough in understanding various physiological events and pathogenesis of diverse diseases. In the fields of diabetes and metabolism, many cellular events associated with the development of disease or its treatment cannot be explained well without taking autophagy into account. While a grand picture of autophagy has been established, detailed aspects of autophagy, particularly that of selective autophagy responsible for homeostasis of specific organelles or metabolic intermediates, are still ambiguous and currently under intensive research. SCOPE OF REVIEW Here, results from previous and current studies on the role of autophagy and its dysregulation in the physiology of metabolism and pathogenesis of diabetes are summarized, with an emphasis on the pancreatic β-cell autophagy. In addition to nonselective (bulk) autophagy, machinery and significance of selective autophagy such as mitophagy of pancreatic β-cells is discussed. Novel findings regarding autophagy types other than macroautophagy are also covered, since several types of autophagy or lysosomal degradation pathways other than macroautophagy coexist in pancreatic β-cells. MAJOR CONCLUSION Autophagy plays a critical role in cellular metabolism, homeostasis of the intracellular environment and function of organelles such as mitochondria and endoplasmic reticulum. Impaired autophagic activity due to aging, obesity or genetic predisposition could be a factor in the development of β-cell dysfunction and diabetes associated with lipid overload or human-type diabetes characterized by islet amyloid deposition. Modulation of autophagy of pancreatic β-cells is likely to be possible in the near future, which would be valuable in the treatment of diabetes associated with lipid overload or accumulation of islet amyloid.

中文翻译：

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β细胞自噬：在β细胞功能障碍中的机制和作用。

背景技术自噬的基本分子机理的阐明是理解各种疾病的各种生理事件和发病机制的突破。在糖尿病和新陈代谢领域，如果不考虑自噬，就无法很好地解释与疾病发展或其治疗有关的许多细胞事件。虽然已经建立了自噬的整体图景，但自噬的具体方面，尤其是负责特定细胞器或代谢中间体稳态的选择性自噬方面，仍然是模棱两可的，目前正在深入研究中。综述的范围在此，总结了以往和当前关于自噬及其失调在糖尿病的代谢生理和发病机制中的作用的研究结果，着重于胰腺β细胞自噬。除了非选择性（批量）自噬外，还讨论了选择性自噬的机制和意义，例如胰腺β细胞的线粒体吞噬。由于大自噬以外的其他自噬类型的新发现也得到了报道，因为胰腺自体胰岛β细胞中共存有几种自噬或溶酶体降解途径，而不是自噬。主要结论自噬在细胞代谢，细胞内环境的稳态以及细胞器如线粒体和内质网的功能中起着关键作用。由于衰老，肥胖或遗传易感性导致的自噬活性受损可能是β细胞功能障碍和与脂质超负荷相关的糖尿病或以胰岛淀粉样蛋白沉积为特征的人型糖尿病的一个因素。