MicroRNA-7 Control of β-Cell Replication

摘要

The study of the insulin-producing pancreatic β-cells transcends the realm of basic biology because of their importance for the maintenance of glucose homeostasis. As their autoimmune-mediated destruction or the impairment of their function cause diabetes, the pursuit of strategies for β-cell replenishment and/or replication is a major objective of regenerative medicine. Owing to their slow turnover in humans, the pancreatic β-cells have been traditionally considered postmitotic (1). However, new evidence supports the notion that β-cells can dynamically adapt their mass and number. This is supported, for instance, by the observation of a perinatal burst of β-cell proliferation (2) or the fact that residual β-cells are found in type 1 diabetic patients decades after diagnosis (3). Although most factors behind this adaptation are pathological (e.g., obesity or hyperglycemia), others are physiological (e.g., pregnancy) (4). Animal models offer us a plethora of examples of β-cell regeneration associated with specific interventions, including duct ligation, β-cell ablation approaches, or partial pancreatectomy (4).