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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 five 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
Brain control of blood glucose levels: implications for the pathogenesis of type 2 diabetes
Presumption of guilt for T cells in type 1 diabetes: lead culprits or partners in crime depending on age of onset?
Kimberly M. Alonge, David A. D’Alessio, Michael W. Schwartz
Alexia Carré, Sarah J. Richardson, Etienne Larger, Roberto Mallone
In this issue, Alonge and colleagues (https://doi.org/10. 1007/s00125-020-05293-3) present a framework for understanding the brain’s role in glucose homeostasis. Their review outlines a crucial role for the brain in sensing blood glucose levels and they cite evidence in support of the concept that defects in this process are fundamental to the pathogenesis of type 2 diabetes. This framework also proposes that the close association between obesity and type 2 diabetes arises from a shared defect in overlapping and highly integrated brain neurocircuitry governing energy homeostasis and glucose homeostasis. The authors highlight the translational potential of this framework by summarising evidence that, in preclinical models of type 2 diabetes, blood glucose levels can be restored to normal in a sustained manner by therapies targeting the brain. They conclude that these considerations suggest that, unlike current non-surgical treatment options, strategies targeting the brain have the potential to induce sustained remission of type 2 diabetes. The figures from this review are available as a downloadable slideset.
It is increasingly recognised that autoimmune type 1 diabetes is a tale of two main characters that both play a role in disease pathogenesis: the T cell and the beta cell. On one hand, the presumption of innocence traditionally granted to beta cells requires revision, as recently reviewed in Diabetologia by Mallone and Eizirik (https://doi.org/10. 1007/s00125-020-05176-7). On the other hand, the presumption of guilt that T cells are often charged with may also need to be reconsidered. In this review, Carré et al (https://doi.org/10.1007/s00125-020-05298-y) evaluate genetic, histopathological, functional and clinical evidence to argue that T cells may behave as ‘lead culprits’ or ‘partners in crime’ in type 1 diabetes, depending on specific disease endotypes, mostly related to age. Increasing evidence points to the existence of a youngeronset endotype with more aggressive autoimmunity and an older-onset endotype with more vulnerable beta cells. Current challenges and opportunities for dissecting this disease heterogeneity are discussed. The figures from this review are available as a downloadable slideset.
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