Role of transcription factors in the transdifferentiation of pancreatic islet cells

The alpha and beta cells act in concert to maintain blood glucose. The a cells release glucagon in response to low levels of glucose to stimulate glycogenolysis in the liver. In contrast, b cells release insulin in response to elevated levels of glucose to stimulate peripheral glucose disposal. Despite these opposing roles in glucose homeostasis, alpha and beta cells are derived from a common progenitor and share many proteins important for glucose sensing and hormone secretion. Results from recent work have underlined these similarities between the two cell types by revealing that beta-to-alpha as well as alpha-to-beta transdifferentiation can take place under certain experimental circumstances. These exciting findings highlight unexpected plasticity of adult islets and offer hope of novel therapeutic paths to replenish beta cells in diabetes. In this review, we focus on the transcription factor networks that establish and maintain pancreatic endocrine cell identity and how they may be perturbed to facilitate transdifferentiation.