• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利:CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验

Effects of cholecystokinin octapeptide and carbachol on neonatal insulin secretory dynamics.

作者信息

Fletcher D J, Rowley W H, Brinn J E

机构信息

Department of Anatomy and Cell Biology, School of Medicine, East Carolina University, Greenville, NC 27858.

出版信息

Regul Pept. 1989 Jun-Jul;25(3):287-93. doi: 10.1016/0167-0115(89)90177-8.

DOI:10.1016/0167-0115(89)90177-8
PMID:2672124
Abstract

The effects of glucose, sulfated cholecystokinin-octapeptide (CCK-8), or carbachol on insulin secretory dynamics were studied in pancreatic islets isolated from 1- and 3-day-old neonatal rats. When challenged with glucose, 1-day islets responded with a definite first phase and elevated secretion during the latter part of the stimulation period; 3-day islets had a first phase and a rising, sustained second phase. The presence of stimulatory concentrations of CCK-8 or carbachol in addition to glucose caused dramatic changes in the release pattern in both islet populations. In 1-day islets, carbachol stimulated mainly first phase secretion whereas CCK-8 enhanced first phase release and produced a definite second phase response. The two secretagogues increased significantly both phases of release in 3-day islets with no differences between the two agents in their effects. These results indicate that CCK-8 and carbachol differentially stimulate neonatal insulin secretion, possibly through different steps in the stimulus-secretion pathway. They also suggest that the cellular mechanism for second phase release is present in 1-day islets and can be activated by CCK-8.

摘要

相似文献

1
Effects of cholecystokinin octapeptide and carbachol on neonatal insulin secretory dynamics.
Regul Pept. 1989 Jun-Jul;25(3):287-93. doi: 10.1016/0167-0115(89)90177-8.
2
Age-dependent stimulation of neonatal insulin release and inositol phosphate accumulation by CCK-8 and carbachol.
Diabetes. 1989 Nov;38(11):1337-42. doi: 10.2337/diab.38.11.1337.
3
Effects of combined secretagogues and extracellular calcium on neonatal insulin release.
Regul Pept. 1990 Feb 4;27(2):237-46. doi: 10.1016/0167-0115(90)90042-u.
4
Involvement of G proteins in the effect of carbachol and cholecystokinin in rat pancreatic islets.G蛋白在卡巴胆碱和胆囊收缩素对大鼠胰岛作用中的参与情况。
Am J Physiol. 1996 Jul;271(1 Pt 1):E65-72. doi: 10.1152/ajpendo.1996.271.1.E65.
5
Effects of short-term culturing on islet phosphoinositide and insulin secretory responses to glucose and carbachol.短期培养对胰岛磷酸肌醇以及胰岛素对葡萄糖和卡巴胆碱分泌反应的影响。
Acta Diabetol. 1995 Oct;32(3):158-64. doi: 10.1007/BF00838485.
6
Ca2+-independent phospholipase A2 contributes to the insulinotropic action of cholecystokinin-8 in rat islets: dissociation from the mechanism of carbachol.钙离子非依赖性磷脂酶A2对大鼠胰岛中胆囊收缩素-8的促胰岛素作用有贡献:与卡巴胆碱的作用机制相分离。
Diabetes. 1998 Sep;47(9):1436-43. doi: 10.2337/diabetes.47.9.1436.
7
Regulation of insulin release by phospholipase C activation in mouse islets: differential effects of glucose and neurohumoral stimulation.磷脂酶C激活对小鼠胰岛胰岛素释放的调节:葡萄糖和神经体液刺激的不同作用
Endocrinology. 1995 Nov;136(11):4903-9. doi: 10.1210/endo.136.11.7588223.
8
Effects of protein kinase C inhibitors on insulin secretory responses from rodent pancreatic islets.蛋白激酶C抑制剂对啮齿动物胰岛胰岛素分泌反应的影响。
Mol Cell Endocrinol. 2001 May 25;177(1-2):95-105. doi: 10.1016/s0303-7207(01)00422-1.
9
Effect of cholecystokinin on the accumulation of inositol phosphates in isolated pancreatic islets.胆囊收缩素对分离的胰岛中肌醇磷酸积累的影响。
Am J Physiol. 1989 Dec;257(6 Pt 1):G865-70. doi: 10.1152/ajpgi.1989.257.6.G865.
10
Effects of CCK-8 on the cytoplasmic free calcium concentration in isolated rat islet cells.
Biochem Biophys Res Commun. 1992 Apr 30;184(2):878-82. doi: 10.1016/0006-291x(92)90672-8.