中华实验外科杂志
中華實驗外科雜誌
중화실험외과잡지
CHINESE JOURNAL OF EXPERIMENTAL SURGERY
2011年
2期
212-214
,共3页
Ghrelin%胰岛素%内向整流钾通道
Ghrelin%胰島素%內嚮整流鉀通道
Ghrelin%이도소%내향정류갑통도
Ghrelin%Insulin%Kir channels
目的 观察外源性Ghrelin对胰岛素分泌和胰岛内向整流钾通道(Kir6.2)表达的影响.方法 Wistar大鼠按10 nmoL/kg的剂量予Ghrelin腹腔注射2周后,分离胰岛进行胰岛素释放实验,分离β细胞检测静息膜电位;检测胰岛Kir6.2 mRNA和蛋白表达变化.结果 在11.1、16.7mmol/L葡萄糖刺激下,对照组的胰岛素释放分别为22.5、43.5 uIU/胰岛/h,Ghrelin组为15.2、30.1uIU/胰岛/h,较对照组显著降低(P<0.05).对照组β细胞的静息膜电位为(-73.2±24.8)mV,Ghrelin组为(-95.4±33.7)mV,较对照组显著降低(P<0.05).而Ghrelin组Kir6.2表达显著高于对照组(P<0.05).结论 Ghrelin与其受体结合后抑制胰岛素分泌,其机制可能与上调Kir6.2表达,使β细胞兴奋性降低有关.
目的 觀察外源性Ghrelin對胰島素分泌和胰島內嚮整流鉀通道(Kir6.2)錶達的影響.方法 Wistar大鼠按10 nmoL/kg的劑量予Ghrelin腹腔註射2週後,分離胰島進行胰島素釋放實驗,分離β細胞檢測靜息膜電位;檢測胰島Kir6.2 mRNA和蛋白錶達變化.結果 在11.1、16.7mmol/L葡萄糖刺激下,對照組的胰島素釋放分彆為22.5、43.5 uIU/胰島/h,Ghrelin組為15.2、30.1uIU/胰島/h,較對照組顯著降低(P<0.05).對照組β細胞的靜息膜電位為(-73.2±24.8)mV,Ghrelin組為(-95.4±33.7)mV,較對照組顯著降低(P<0.05).而Ghrelin組Kir6.2錶達顯著高于對照組(P<0.05).結論 Ghrelin與其受體結閤後抑製胰島素分泌,其機製可能與上調Kir6.2錶達,使β細胞興奮性降低有關.
목적 관찰외원성Ghrelin대이도소분비화이도내향정류갑통도(Kir6.2)표체적영향.방법 Wistar대서안10 nmoL/kg적제량여Ghrelin복강주사2주후,분리이도진행이도소석방실험,분리β세포검측정식막전위;검측이도Kir6.2 mRNA화단백표체변화.결과 재11.1、16.7mmol/L포도당자격하,대조조적이도소석방분별위22.5、43.5 uIU/이도/h,Ghrelin조위15.2、30.1uIU/이도/h,교대조조현저강저(P<0.05).대조조β세포적정식막전위위(-73.2±24.8)mV,Ghrelin조위(-95.4±33.7)mV,교대조조현저강저(P<0.05).이Ghrelin조Kir6.2표체현저고우대조조(P<0.05).결론 Ghrelin여기수체결합후억제이도소분비,기궤제가능여상조Kir6.2표체,사β세포흥강성강저유관.
Objective To investigate the influence of ghrelin administration on the insulin secretion, and the expression of Kir6. 2 channels in islets. Methods Ghrelin was intraperitoneally administrated in Wistar rats at the doses 10 nmol/kg every day for 2 weeks. Islets were isolated for insulin release experiments. Single β cells were isolated for electrophysiological experiments. Meanwhile, the expression levels of Kir6. 2 mRNA and protein in islets were detected. Results At 11. 1 and 16. 7 mmol/L glucose,the levels of insulin release in control group were 22. 5 and 43.5 uIU/islet per h, and those in ghrelin-treated group were 15. 2 and 30. 1 uIU/islet per h (P <0. 05 ). In control group, the resting membrane potential reached ( - 73.2 ± 24. 8 ) mV, but in ghrelin-treated group, it was hyperpolarized to ( - 95.4 ± 33.7 )mV ( P < 0. 05 ). The Kir6. 2 expression levels were significantly up-regulated by ghrelin ( P < 0. 05 ).Conclusion Ghrelin via pancreatic GHSR up-regulates the Kir6. 2 expression in islets, hyperpolarizing the resting membrane potential, and resulting in the inhibition of insulin release.