Knut Dahl-Jørgensen’s group has recently published two new articles in Diabetologia with interesting results from the DiViD-study. Shiva et al have compared the expression of IL-1β, which is considered to be a key mediator of beta cell destruction, in the pancreatic biopsies from DiViD with its expression in cadaveric pancreas sections from non-diabetic autoantibody-positive and -negative individuals and those with long-standing disease ( The key question raised in the article was whether or not IL-1β is expressed within and around islets of Langerhans during early type 1 diabetes (T1D). Maybe surprisingly, a low number of IL-1β positive cells were present in and around islets in the biopsies from the DiViD-cases. This indicates that successful clinical prevention of T1D may require blockade of as-yet unidentified multiple beta cell destructive pathways.

Holm et al investigated whether sphingolipid metabolism may contribute to the pathogenesis of human T1D and whether increasing the levels of the sphingolipid sulfatide would prevent models of diabetes in NOD mice ( Sphingolipids are known to play important roles in beta cell physiology, by regulating proinsulin folding and insulin secretion and in controlling apoptosis. The key question raised in this article was whether or not sphingolipid metabolism is altered in newly diagnosed patients with T1D. To answer this, the biopsies from DiViD-cases were examined by immunohistochemistry and immunofluorescence, and RNA was extracted from well-kept frozen biopsies for transcriptional analysis to evaluate the expression of sphingolipid-related genes. Interestingly, we observed a loss of sulfatide and reduced expression of enzymes involved in sphingolipid metabolism in the DiViD-cases. In addition, increasing sulfatide levels by fenofibrate protected against experimental diabetes in NOD mice. In combination, these seminal data suggest that modulation of sphingolipid metabolism could be used to prevent and treat T1D.