Farshori P Q, Goode D
Department of Zoology, University of Maryland, College Park 20742.
J Submicrosc Cytol Pathol. 1994 Apr;26(2):137-46.
Hamster islet tumor (HIT) cells retain much of the capacity of normal beta cells to act as glucose sensors. When stimulated with glucose or glucose plus forskolin, HIT cells release much more insulin than unstimulated cells. Ultrastructural analysis reveals that the secretory product of these cells is stored in membrane-bound granules that associate with microtubules under certain circumstances. Immunofluorescence studies using insulin antibody confirm the presence of insulin in granular structures in these cells. The microtubule inhibitor Nocodazole reduces the number of polymerized microtubules and inhibits the sustained phase of insulin secretion in HIT cells. Thus, the structural integrity of microtubules is important for the sustained phase of the insulin secretion to occur. The microtubule stabilizing drug taxol does not decrease insulin secretion. Since taxol blocks microtubule depolymerization, microtubule polymerization-depolymerization alone does not appear to be responsible for insulin granule transport. The increased use of these drugs in cancer research and therapy makes it important to understand their effects on insulin secretion.
仓鼠胰岛瘤（HIT）细胞保留了许多正常β细胞作为葡萄糖传感器的能力。当用葡萄糖或葡萄糖加福斯高林刺激时，HIT细胞释放的胰岛素比未刺激的细胞多得多。超微结构分析表明，这些细胞的分泌产物储存在膜结合颗粒中，在某些情况下，这些颗粒与微管相关联。使用胰岛素抗体的免疫荧光研究证实了这些细胞的颗粒结构中存在胰岛素。微管抑制剂诺考达唑减少了聚合微管的数量，并抑制了HIT细胞中胰岛素分泌的持续阶段。因此，微管的结构完整性对于胰岛素分泌的持续阶段的发生很重要。微管稳定药物紫杉醇不会减少胰岛素分泌。由于紫杉醇阻止微管解聚，仅微管聚合 - 解聚似乎并不负责胰岛素颗粒的运输。这些药物在癌症研究和治疗中的使用增加，使得了解它们对胰岛素分泌的影响变得很重要。
