1932

Abstract

Abstract

Once thought incapable of significant proliferation, the pancreatic β-cell has recently been shown to harbor immense powers of self-renewal. Pancreatic β-cells, the sole source of insulin in vertebrate animals, can grow facultatively to a degree unmatched by other organs in experimental animals. β-cell growth matches changes in systemic insulin demand, which increase during common physiologic states such as aging, obesity, and pregnancy. Compensatory changes in β-cell mass are controlled by β-cell proliferation. Here we review recent advances in our understanding of the intrinsic factors and mechanisms that control β-cell cycle progression. Dysregulation of β-cell proliferation is emerging as a fundamental feature in the pathogenesis of human disease states such as cancer and diabetes mellitus. New experimental observations and studies of these diseases suggest that β-cell fate and expansion are coordinately regulated. We speculate on how these advances may accelerate the discovery of new strategies for the treatment of diseases characterized by a deficiency or excess of β-cells.

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/content/journals/10.1146/annurev.cellbio.22.010305.104425
2006-11-10
2024-07-15
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Supplementary Data

  • Article Type: Review Article
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