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Pancreatic beta cell autophagy is impaired in type 1 diabetes – published online 30/01/2021

muralidharan graphical abstract

Charanya Muralidharan, Abass M. Conteh, Michelle R. Marasco, Justin J. Crowder, Jeroen Kuipers, Pascal de Boer, Amelia K. Linnemann

Autophagy is a degradation process in which excessive or damaged cellular materials are degraded and recycled. This degradative process has been shown to promote beta cell homeostasis and proliferation and, also, to protect against apoptosis. Crinophagy is a specialised form of autophagy where secretory granules directly fuse with lysosomes and get degraded. Prior studies have reported impaired autophagy in the context of type 2 diabetes; however, it is unknown if islet autophagy is impaired in type 1 diabetes. In this issue, Muralidharan et al (https://doi.org/10.1007/s00125-021-05387-6) provide evidence of impairment in autophagy in the islets of diabetic NOD mice, as well as impairment of both autophagy and crinophagy in the beta cells of human organ donors with type 1 diabetes. Additionally, the authors report an accumulation of telolysosomes in the beta cells of autoantibody-positive donors, suggesting that lysosomal defects are present prior to the onset of clinical hyperglycaemia. The authors conclude that these findings indicate that the beta cell autophagy and crinophagy impairments observed in type 1 diabetes could be, at least in part, due to defective lysosomes in the prediabetic phase of disease development.

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