Pancreatic cell fate specification: insights into developmental mechanisms and their application for lineage reprogramming

Abstract

Diabetes is a group of metabolic disorders, which results from insufficient functional pancreatic β-cell mass either due to the autoimmune destruction of insulin producing β-cells, or their death or de-differentiation as compensation for insulin resistance. The ability to reprogram cell types within close developmental proximity to β-cells offers a strategy to replenish β-cell mass and a future possible treatment of diabetes. Here, we review recent advances in the fields of pancreas development and lineage reprogramming. We also probe the possibility of using reprogrammed cells as an approach by which to further understand developmental mechanisms, in particular roadblocks to changing cell identity. Finally, we highlight fundamental challenges that need to be overcome to advance lineage reprogramming for generating pancreatic cells.