中文摘要：

目的观察双孔钾通道KCNKl6在大鼠胰岛中的表达情况，并探讨促进G细胞胰岛素分泌的刺激因素对其表达的调节。方法采用实时定量PCR和组织化学染色技术观察KCNKl6在大鼠胰岛及其他组织中的表达。分别用葡萄糖、催乳素、软脂酸以及曲古菌素A（TrichostatinA．TSA）处理大鼠胰岛24h，实时定量PCR和Western印迹法检测KCNKl6的表达水平。以ELISA检测TSA处理大鼠胰岛24h后葡萄糖和KCl刺激的胰岛素分泌水平。不同浓度和时间的TSA处理INSl-E细胞．实时定量PCR检测KCNKl6的表达水平。结果KCNKl6在大鼠胰岛中高表达。葡萄糖、催乳素和脂肪酸并不影响大鼠胰岛KCNKl6的表达。TSA显著增强大鼠胰岛葡萄糖和KCl刺激的胰岛素分泌（P〈0．05），同时显著下调KCNKl6的mRNA和蛋白表达（P〈0．01）。在INSl-E细胞，TSA抑制KCNKl6的表达作用呈浓度和时间依赖性（P〈0．05）。结论KCNKl6在大鼠胰岛中特异性高表达，且其表达水平能被TSA显著下调．KCNKl6表达的下调有可能介导了TSA增强的胰岛素分泌．

英文摘要：

Objective To observe the expression of a two-pore domain K＋ channel KCNK16 in rat islets, and to explore its regulation by insulin secretagogues. Methods Real time-PCR and immunohistoehemistry were employed to observe the expression of KCNK16 in rat islets and other tissues. Rat islets were exposed to glucose, prolactin, palmitate, and trichostatin A （TSA） for24 h and KCNK16 expression were determined by reahime-PCR and Western blot. Glucose- and KCl-stimulated insulin secretion were assayed by ELISA after islets were exposed to TSA for 24 h. The dose- and time-dependent effects of TSA on KCNK16 expression in INS1 -E cells were determined by RT- PCR. Results KCNK16 was highly expressed in rat islets. Glucose, prolactin, and palmitate did not affect the expression of KCNK16 in rat islets. TSA treatment significantly potentiated glucose- and KCl-stimulated insulin secretion in isolated rat islets （ P 〈 0.05 ）, along with decreased KCNK16 mRNA and protein expressions （ P 〈 O. 01 ）. TSA inhibited KCNK16 expression in a dose- and time-dependent manner in INS1-E cells （P 〈 0.05 ）. Conclusion KCNK16 is exclusively and highly expressed in rat islets and its expression can be down-regulated by TSA treatment. It is possible that TSA enhances insulin secretion via decreasing KCNK16 expression.