MicroRNA-7 Control of β-Cell Replication

  1. Ricardo L. Pastori
  1. Diabetes Research Institute, University of Miami Leonard M. Miller School of Medicine, Miami, Florida
  1. Corresponding author: Ricardo L. Pastori, rpastori{at}

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). In this issue of Diabetes, Wang et al. (5) describe the proliferation of β-cells induced by regulation of the mTOR pathway through microRNA-7 (miR-7). MicroRNAs (miRNAs) are noncoding gene products that posttranscriptionally regulate gene expression (6). miRNAs recognize and bind to partially complementary sequences on the RNA’s 3′UTR, inhibiting its expression by translation repression or degradation. …

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