期刊文献+

可乐定置换物对正常小鼠离体胰岛功能的影响

Effects of clonidine-displacing substance on the function of isolated islets from normal mice
下载PDF
导出
摘要 目的 探讨可乐定置换物 (CDS)对胰岛功能的影响。方法 胶原酶和DNA酶联合消化法分离NMRI小鼠胰岛 ,RPMI1 640组织培养液过夜培养 ,采用MilliporeMultiscreen系统观察CDS对胰岛功能的影响。放免法测定孵育液中胰岛素及胰高糖素的浓度。结果  (1 )离体胰岛胰高糖素的分泌明显受葡萄糖浓度的抑制 ,CDS显著抑制胰高糖素的分泌 ,且抑制强度明显依赖于CDS的浓度。 (2 )离体胰岛胰岛素的分泌依赖于孵育液中的葡萄糖浓度 ,CDS明显刺激胰岛素的释放。Ca2 + 通道阻滞剂硝苯吡啶 (2 5μmol·L- 1 )及K+ 通道开放剂二氮嗪(1 0 0 μmol·L- 1 )可显著抑制胰岛素释放 ,但其作用可被CDS废除。结论 作为咪唑啉受体的内源性配体 ,CDS可刺激离体胰岛胰岛素的释放 。 Objective To research the effects of the clonidine-displacing substance (CDS) on the function of the islets. Methods The islets of NMRI mice were isolated by digestion combined with collagenase and DNase, incubated in RPMI 1640 tissue culture medium overnight. The experiments were completed with Millipore Multiscreen Assay System. The level of insulin and glucagon were measured by RIA. Results (1) Glucagon secretion of the isolated islets in incubation medium was inhibited by glucose. CDS could also inhibit glucagon secretion of the islets significantly, and the inhibitory effects was concentration-dependent. (2) Insulin secretion of the isolated islets in incubation medium was glucose concentration-dependent positively.The CDS could stimulate insulin secretion of the islets significantly. Nifedipine (Ca 2+ channel blocker) and diazoxide (K + channel opener) could inhibit the insulin release, but their effects could be abolished by CDS.Conclusion As an endogenous ligand of imidazoline receptors, CDS could stimulate insulin secretion, and inhibit glucagon release in the isolated islets.
出处 《新乡医学院学报》 CAS 2002年第3期158-160,共3页 Journal of Xinxiang Medical University
基金 本研究由国家留学基金资助 (98941 0 60 )
关键词 可乐定置换物 小鼠 离体胰岛 胰高血糖素 胰岛素 clonidine-displacing substance isolated islets mice glucagon insulin
  • 相关文献

参考文献1

二级参考文献8

  • 1[1]Lacy P E, Kostianovsky M. Methods for the isolation of intact islets of Langerhans from the rat pancreas[J ]. Diabetes , 1975,24 (5):961-970.
  • 2[2]Panten U, Schwanstecher M, Schwanstecher C. Sulfonylurea receptors and mechanism of sulfonylurea action [J]. Exp Clin Endocrinol Diabetes, 1996,104( 1 ): 1 - 9.
  • 3[3]Rustenbeck 1, Kopp M, Ratzka P, et al. Imidazolines and the pancreatic B- cell actions and binding sites[J]. Ann N Y Acad Sci , 1999,881(6): 229 - 240.
  • 4[4]Morgan NG, Chan SLF, Brown CA, et al . Characterization of the imidazoline binding site involved in regulation of insulin secretion[J ]. Ann N Y Acad Sci, 1999,881(6) :361 - 373.
  • 5[5]Zaitsev SV, Efanov AE, Efanov IB, et al . Imidazoline compounds stimulate insulin release by inhibition of KATP channels and interaction with the exocytotic machinery[J]. Diabetes , 1996,45( 11 ): 1610 - 1618.
  • 6[6]Lefebvre PJ. Glucagon and its family, revisted[J]. Diabetes Care , 1995,18(5) :715 - 730.
  • 7[7]Bokvist K, Olsen HL, Hψy M, et al . Characterization of sulfonylurea and ATP- regulated K+ channels in rat pancreatic A- cells[J ]. Eur J Physiol, 1999, 438(7) :428 - 436.
  • 8[8]Hψy M, Bokvist K, Weng XG, et al . Phentolamine inhibits exocytosis of glucagon by Gi2 protein - dependent activation of calcineurin in rat pancreatic α - cells[J]. J Boil Chem ,2001,276(2) :925 - 930.

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部