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首页> 外文期刊>Cell cycle >Control of pancreatic beta-cell fate by insulin signaling: The sweet spot hypothesis.
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Control of pancreatic beta-cell fate by insulin signaling: The sweet spot hypothesis.

机译：通过胰岛素信号传导控制胰岛β细胞命运：最佳假设。

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摘要

Diabetes results from an absolute or relative deficiency in functional pancreatic beta-cell mass. Over the past few years, there has been renewed interest in the role of insulin itself in the regulation of beta-cell fate. Numerous animal models point to a critical role for beta-cell insulin signaling in the survival and proliferation of pancreatic beta-cells. In the present article, we review new studies that elucidate the mechanism by which insulin exerts anti-apoptotic and pro-mitogenic effects on beta-cells. In particular, we highlight the emerging role for Raf-1 kinase in autocrine insulin signaling and beta-cell fate decisions. We also discuss provocative evidence that the relationship between the dose of insulin and the birth and death of beta-cells is not linear. We propose a new hypothesis based on these findings, called the 'sweet spot' hypothesis, that can explain how both upward and downward deviations from normal levels of autocrine/paracrine insulin signaling might play an important role in the pathogenesis of type 1 diabetes and type 2 diabetes. We also highlight the key experiments that are required to further test this hypothesis.
机译：糖尿病是由功能性胰腺β细胞量的绝对或相对缺乏引起的。在过去的几年中，人们对胰岛素本身在调节β细胞命运中的作用重新产生了兴趣。许多动物模型都指出β细胞胰岛素信号在胰腺β细胞存活和增殖中起着关键作用。在本文中，我们回顾了阐明胰岛素对β细胞发挥抗凋亡和促有丝分裂作用的机制的新研究。特别是，我们强调了Raf-1激酶在自分泌胰岛素信号传导和β细胞命运决定中的新兴作用。我们还讨论了刺激性证据，即胰岛素剂量与β细胞的出生与死亡之间的关系不是线性的。基于这些发现，我们提出了一个新的假设，称为“最佳点”假设，该假设可以解释自分泌/旁分泌胰岛素信号正常水平的向上和向下偏离可能如何在1型糖尿病和2型糖尿病的发病机理中发挥重要作用。 2糖尿病。我们还重点介绍了进一步检验该假设所需的关键实验。

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