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Competition for publication in Diabetologia continues to grow, and less than 20% of papers are accepted. Of all the high-quality papers that appear in this month’s issue I want to draw your attention to the articles that I think are particularly interesting. The articles are summarised here. Our publisher, Springer, has kindly made the full text of each of these papers freely available. I hope you enjoy reading them! Sally M. Marshall, Editor

The pancreas in health and disease The focus of this year’s special issue is ‘The pancreas in health and in diabetes’, introduced in an editorial (https://doi.org/10. 1007/s00125-020-05235-z). Atkinson et al (https://doi.org/10. 1007/s00125-020-05203-7) begin by reviewing the current evidence on human pancreatic anatomy and the changes that occur in individuals with type 1 or type 2 diabetes. Jennings and colleagues (https://doi.org/10.1007/s00125-020-05161-0) go on to discuss how alterations in important steps in the development of the mammalian pancreas may contribute to the abnormalities seen in diabetes. Abnormal insulin production by the pancreas underlies the pathogenesis of diabetes, and Vasiljević and coauthors (https://doi.org/10. 1007/s00125-020-05192-7) outline the post-transcriptional mechanisms regulating insulin production and how their deficits can cause diabetes. The sole source of circulating insulin is the pancreatic beta cell. In their review, Rutter et al (https:// doi.org/10.1007/s00125-020-05205-5) discuss the specialisations that allow this cell to perform its unique role. Autoimmune beta cell destruction results in type 1 diabetes and Mallone and Eizirik (https://doi.org/10.1007/s00125-02005176-7) consider why beta cells are vulnerable autoimmune targets. Esser et al (https://doi.org/10.1007/s00125-02005245-x) go on to describe models to explain the pathogenesis of hyperglycaemia in type 2 diabetes. Age is one of the main risk factors for developing type 2 diabetes and Cristina Aguayo-Mazzucato (https://doi.org/10.1007/ s00125-020-05185-6) summarises the functional changes

that occur in ageing beta cells. Diabetes can also occur as a consequence of a wide variety of exocrine pancreas diseases, as discussed by Rickels et al (https://doi.org/10.1007/s00125020-05210-8). Redondo et al (https://doi.org/10.1007/ s00125-020-05211-7) propose a paradigm to help explain the heterogeneity within and between diabetes types, concluding that this new approach may facilitate personalised medicine in diabetes. In their review, Bellin and Dunn (https://doi.org/10.1007/s00125-020-05184-7) detail the variety of transplant strategies available for individuals with type 1 diabetes. Looking more closely at the islet itself, Mark Huising (https://doi.org/10.1007/ s00125-020-05213-5) describes the cellular components of this special structure that are important to its role. Moede et al (https://doi.org/10.1007/s00125-020-05196-3) focus specifically on the importance of islet alpha cell–beta cell communication for glucose homeostasis, while Almaça et al (https://doi.org/10.1007