Suppr超能文献

确定负责葡萄糖刺激胰岛素分泌第一阶段的对接颗粒池。

Identification of the docked granule pool responsible for the first phase of glucose-stimulated insulin secretion.

作者信息

Daniel S, Noda M, Straub S G, Sharp G W

机构信息

Department of Molecular Medicine, College of Veterinary Medicine, Cornell University, Ithaca, New York 14853-6401, USA.

出版信息

Diabetes. 1999 Sep;48(9):1686-90. doi: 10.2337/diabetes.48.9.1686.

Abstract

The mechanisms underlying the first phase of glucose-stimulated insulin release, the deterioration of which marks the early stages of both type 1 and type 2 diabetes, are essentially unknown. Among many hypotheses, one holds that the first phase is due to a readily releasable pool of insulin-containing granules. We used current knowledge of the mechanisms of exocytosis and the proteins involved in docking granules at the plasma membrane to test this hypothesis. A docked pool of readily releasable granules was identified by immunoprecipitation of the plasma membrane protein syntaxin with a specific antibody and by co-immunoprecipitation of soluble N-ethylmaleimide-sensitive factor attachment protein-25 (SNAP-25) and the granule proteins synaptobrevin and synaptotagmin. The four SNARE proteins co-immunoprecipitated each other, thus identifying the core complex associated with docked granules. Using co-immunoprecipitation as a marker for docked granules, we found that the docked pool was rapidly discharged during the first phase of glucose-stimulated insulin release and refilled during the second phase. Other secretagogues also released the pool, whereas the physiological inhibitor norepinephrine blocked its release. Further studies on the nature of this pool of granules should shed light on the causes of its deterioration in the early stages of diabetes and the reasons for deficient insulin release.

摘要

葡萄糖刺激的胰岛素释放第一阶段的潜在机制基本上仍不清楚,而该阶段机制的恶化标志着1型和2型糖尿病的早期阶段。在众多假说中,有一种认为第一阶段是由于存在一个易于释放的含胰岛素颗粒池。我们利用当前关于胞吐作用机制以及参与颗粒停靠在质膜上的蛋白质的知识来检验这一假说。通过用特异性抗体免疫沉淀质膜蛋白 syntaxin 以及共免疫沉淀可溶性N - 乙基马来酰亚胺敏感因子附着蛋白25(SNAP - 25)和颗粒蛋白突触囊泡蛋白及突触结合蛋白,确定了一个停靠的易于释放颗粒池。这四种SNARE蛋白相互共免疫沉淀,从而确定了与停靠颗粒相关的核心复合物。以共免疫沉淀作为停靠颗粒的标志物,我们发现该停靠池在葡萄糖刺激的胰岛素释放第一阶段迅速排空,并在第二阶段重新填充。其他促分泌剂也能释放该颗粒池,而生理抑制剂去甲肾上腺素则会阻断其释放。对这一颗粒池性质的进一步研究应能阐明其在糖尿病早期恶化的原因以及胰岛素释放不足的原因。

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验