β-Cell differentiation and regeneration in type 1 diabetes

• Published in: Diabetes, obesity & metabolism Vol. 15; no. s3; pp. 98 - 104
• Main Authors: Ding, L., Gysemans, C., Mathieu, C.
• Format: Journal Article
• Language: English
• Published: Oxford, UK Blackwell Publishing Ltd 01.09.2013
• Subjects: Animals; Cell Differentiation; Cell Proliferation; Cell Transdifferentiation - physiology; Diabetes Mellitus, Type 1 - pathology; Diabetes Mellitus, Type 1 - physiopathology; Humans; Insulin-Secreting Cells - pathology; Insulin-Secreting Cells - physiology; Islets of Langerhans - pathology; Islets of Langerhans - physiology; regeneration; Regeneration - physiology; replication; reprogramming; type 1 diabetes; β-cells; replication; reprogramming; type 1 diabetes; regeneration; β-cells
• ISSN: 1462-8902; 1463-1326; 1463-1326
• DOI: 10.1111/dom.12164

Pancreatic insulin‐producing β‐cells have traditionally been viewed as a quiescent cell population. However, several recent lines of evidence indicated that like most tissues the β‐cell mass is dynamically regulated with ongoing β‐cell regeneration throughout life to replenish lost or damaged β‐cells. In type 1 diabetes (T1D), this fine‐tuned balance between β‐cell death and β‐cell renewal in the endocrine pancreas is lost and the deficit in β‐cell mass is largely caused by autoimmune‐mediated apoptosis. Currently, the concept that a cure for T1D will require both re‐establishment of immunological tolerance along with replacement or regeneration of a functional β‐cell mass in T1D patients is generally accepted. In this study our current understanding of the events directing β‐cell replication, β‐cell reprogramming from different cell types and β‐cell regeneration is reviewed, in view of the results of various immunomodulatory strategies aiming at blocking autoimmune responses against pancreatic β‐cells and at improving β‐cell mass and function in subjects with T1D.