From pancreatic islet formation to beta-cell regeneration

Abstract

Diabetes mellitus represents a major healthcare burden and, due to the increasing prevalence of type I diabetes and the complications arising from current treatments, other alternative therapies must be found. Type I diabetes arises as a result of a cell-mediated autoimmune destruction of insulin producing pancreatic β-cells. Thus, a cell replacement therapy would be appropriate, using either in vitro or in vivo cell differentiation/reprogramming from different cell sources. Increasing our understanding of the molecular mechanisms controlling endocrine cell specification during pancreas morphogenesis and gaining further insight into the complex transcriptional network and signaling pathways governing β-cell development should facilitate efforts to achieve this ultimate goal, that is to regenerate insulin-producing β-cells. This review will therefore describe briefly the genetic program underlying mouse pancreas development and present new insights regarding β-cell regeneration.