Department of Pharmacology, University of Oxford, Mansfield Road, Oxford, UK.
Islets. 2010 Sep-Oct;2(5):323-30. doi: 10.4161/isl.2.5.12747. Epub 2010 Sep 1.
Several recent reports, including one in this journal, have reignited the debate about whether the calcium-mobilizing messenger, nicotinic adenine nucleotide diphosphate (NAADP) plays a central role in the regulation of calcium signalling in pancreatic β-cell. These studies have highlighted a role for NAADP-induced Ca(2+) mobilization not only in mediating the effects of the incretin, GLP-1 and the autocrine proliferative effects of insulin, but also possibly a fundamental role in glucose-mediated insulin secretion in the pancreatic β-cell.
最近有几项报告，包括本刊上的一篇，再次引发了关于钙动员信使烟碱腺嘌呤二核苷酸（NAADP）是否在调节胰腺β细胞钙信号中起核心作用的争论。这些研究强调了 NAADP 诱导的 Ca(2+)动员不仅在介导肠降血糖素 GLP-1 的作用和胰岛素的自分泌增殖作用中起作用，而且可能在葡萄糖介导的胰腺β细胞胰岛素分泌中起基本作用。
