当前位置: Nature » 生物医学 » 正文


摘要 : 中国香港中文大学等处的研究人员在新研究中,解释了为什么囊性纤维化患者随着年龄增长经常会患糖尿病。相关文章发表于2014年7月15日的《Nature Communications》杂志上。


现在,Hsiao Chang Chan及同事发现,CFTR还在胰脏中表达,在那里它调控胰岛素在葡萄糖诱导下从β-细胞中的分泌。他们进而显示,用于治疗囊性纤维化的一种实验药物能恢复发生这一突变的β-细胞的正常功能。



Glucose-induced electrical activities and insulin secretion in pancreatic islet β-cells are modulated by ​CFTR

Jing Hui Guo, Hui Chen, Ye Chun Ruan, Xue Lian Zhang, Xiao Hu Zhang, Kin Lam Fok, Lai Ling Tsang, Mei Kuen Yu, Wen Qing Huang, Xiao Sun, Yiu Wa Chung, Xiaohua Jiang,Yoshiro Sohma & Hsiao Chang Chan

The cause of insulin insufficiency remains unknown in many diabetic cases. Up to 50% adult patients with cystic fibrosis (CF), a disease caused by mutations in the gene encoding the ​CF transmembrane conductance regulator (​CFTR), develop CF-related diabetes (CFRD) with most patients exhibiting ​insulin insufficiency. Here we show that ​CFTR is a regulator of ​glucose-dependent electrical acitivities and insulin secretion in β-cells. We demonstrate that ​glucose elicited whole-cell currents, membrane depolarization, electrical bursts or action potentials, Ca2+ oscillations and insulin secretion are abolished or reduced by inhibitors or knockdown of ​CFTR in primary mouse β-cells or RINm5F β-cell line, or significantly attenuated in ​CFTR mutant (DF508) mice compared with wild-type mice. ​VX-809, a newly discovered corrector of DF508 mutation, successfully rescues the defects in DF508 β-cells. Our results reveal a role of ​CFTR in ​glucose-induced electrical activities and ​insulin secretion in β-cells, shed light on the pathogenesis of CFRD and possibly other idiopathic diabetes, and present a potential treatment strategy.

来源: Nature中文 浏览次数:27


RSS订阅 - 填写您的邮件地址,订阅我们的精彩内容: - 网站地图
网站联系电话:020-87540820 备案号:粤ICP备11050685号-8 增值电信业务经营许可证:粤B2-20120479
©2011-2015 生物帮 All rights reserved.