Type 1 diabetes is caused by the loss of insulin-producing β-cells as a result of an autoimmune condition. Despite current therapeutic approaches aimed at restoring the insulin supply, complications caused by variations in glycaemia may still arise with age. There is therefore mounting interest in the establishment of alternative therapies. Most current approaches consist in designing rational protocols for in vitro or in vivo cell differentiation/reprogramming from a number of cell sources, including stem, progenitor or differentiated cells. Towards this ultimate goal, it is clear that we need to gain further insight into the interplay between signalling events and transcriptional networks that act in concert throughout pancreatic morphogenesis. This short review will therefore focus on the main events underlying pancreatic development with particular emphasis on the genetic determinants implicated, as well as on the relatively new concept of endocrine cell reprogramming, that is the conversion of pancreatic α-cells into cells displaying a β-cell phenotype.
© 2011 Blackwell Publishing Ltd.