Institut de Recherche en Cancérologie de Montpellier, France.
Islets. 2010 Jan-Feb;2(1):51-3. doi: 10.4161/isl.2.1.10338.
Pancreatic β-cells are sensors of circulating glucose levels that control insulin secretion through a finely-tuned process. Under hyperglycemic conditions, glucose enters the cell, generates ATP, leading to a subsequent closure of voltage-dependent ATP channels, membrane depolarization, Ca²(+) entry and exocytosis of insulin vesicles. In pathological conditions, such as during type 2 diabetes (T2D), chronic hyperglycemia will ultimately result in decreased capability of β-cells to secrete sufficient amount of insulin to regulate glycemia. Therefore, understanding of the mechanisms of modulation of insulin secretion could be of interest for the treatment of diabetes. We have demonstrated that a particular cell cycle regulator, E2F1, is involved in pancreatic post-natal growth through its functions in the control of β-cell proliferation. Based on the observation that cell cycle regulators were highly expressed in non-proliferating β-cell, we hypothesized that these proteins could also have a direct role in pancreatic β-cell function. Altogether our data unravel a new function for these factors in the control of insulin secretion and open up new avenues for the treatment of diabetes.
胰岛 β 细胞是循环血糖水平的传感器，通过精细调节的过程控制胰岛素分泌。在高血糖条件下，葡萄糖进入细胞，产生 ATP，导致随后电压依赖性 ATP 通道关闭、膜去极化、Ca²(+)内流和胰岛素囊泡的胞吐作用。在病理条件下，如 2 型糖尿病 (T2D) 中，慢性高血糖最终会导致 β 细胞分泌足够量胰岛素以调节血糖的能力下降。因此，了解调节胰岛素分泌的机制可能对糖尿病的治疗具有重要意义。我们已经证明，特定的细胞周期调节剂 E2F1 通过控制 β 细胞增殖参与胰腺出生后生长。基于观察到细胞周期调节剂在非增殖的 β 细胞中高度表达，我们假设这些蛋白质也可以在胰腺 β 细胞功能中发挥直接作用。总的来说，我们的数据揭示了这些因素在控制胰岛素分泌中的新功能，并为糖尿病的治疗开辟了新的途径。
