Once thought incapable of significant proliferation, the pancreatic beta-cell has recently been shown to harbor immense powers of self-renewal. Pancreatic beta-cells, the sole source of insulin in vertebrate animals, can grow facultatively to a degree unmatched by other organs in experimental animals. beta-cell growth matches changes in systemic insulin demand, which increase during common physiologic states such as aging, obesity, and pregnancy. Compensatory changes in beta-cell mass are controlled by beta-cell proliferation. Here we review recent advances in our understanding of the intrinsic factors and mechanisms that control beta-cell cycle progression. Dysregulation of beta-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 beta-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 beta-cells.

中文翻译：

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胰腺β细胞增殖的内在调节剂。

曾经被认为无法显着增殖的胰岛β细胞最近被证明具有巨大的自我更新能力。胰腺β细胞是脊椎动物中胰岛素的唯一来源，它可以兼性地生长到实验动物中其他器官无法比拟的程度。β细胞的生长与全身性胰岛素需求的变化相匹配，而这种变化在常见的生理状态（例如衰老，肥胖和怀孕）中会增加。β细胞质量的补偿性变化受β细胞增殖的控制。在这里，我们回顾了对控制β细胞周期进程的内在因素和机制的最新进展。β细胞增殖失调正在成为人类疾病如癌症和糖尿病的发病机理中的基本特征。对这些疾病的新实验观察和研究表明，β细胞的命运和扩增受到协调调节。我们推测这些进展如何加速发现以β细胞缺乏或过多为特征的疾病的新治疗策略。