Wagoner P K, Chen C, Worley J F, Dukes I D, Oxford G S
Department of Cell Physiology and Biophysics, Glaxo Research Institute, Glaxo, Inc., Research Triangle Park, NC 27709.
Proc Natl Acad Sci U S A. 1993 Oct 1;90(19):9145-9. doi: 10.1073/pnas.90.19.9145.
The release of insulin from the pancreatic beta cell is dependent upon a complex interplay between stimulators and inhibitors. Recently, amylin, a peptide secreted by pancreatic beta cells, has been implicated in the development of type II (noninsulin dependent) diabetes through its modulation of the peripheral effects of insulin. However, the effect of amylin on insulin secretion from the beta cell has remained controversial. It is reported here that in single beta cells exhibiting normal glucose sensing, amylin causes membrane hyperpolarization, increases in net outward current, and reductions in insulin secretion. In contrast, in cells with abnormal glucose sensing (e.g., from db/db diabetic mice), amylin has no effect on electrical activity or secretion. Thus, amylin's effects on excitation-secretion coupling in the beta cell of the pancreas appear to be linked to the cell's capacity for normal glucose sensing.
胰岛素从胰腺β细胞的释放取决于刺激物和抑制剂之间复杂的相互作用。最近，胰岛淀粉样多肽，一种由胰腺β细胞分泌的肽，通过调节胰岛素的外周作用，与II型（非胰岛素依赖型）糖尿病的发生有关。然而，胰岛淀粉样多肽对β细胞胰岛素分泌的影响仍存在争议。本文报道，在表现出正常葡萄糖感知的单个β细胞中，胰岛淀粉样多肽会导致膜超极化、净外向电流增加以及胰岛素分泌减少。相反，在葡萄糖感知异常的细胞（例如来自db/db糖尿病小鼠）中，胰岛淀粉样多肽对电活动或分泌没有影响。因此，胰岛淀粉样多肽对胰腺β细胞兴奋-分泌偶联的影响似乎与细胞正常葡萄糖感知的能力有关。
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