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为什么囊性纤维化患者随着年龄增长经常会患糖尿病

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。

囊性纤维化是由“CFTR”基因的突变引起的,这些突变导致粘液在肺中积累。流行病学研究表明,囊性纤维化患者经常会患糖尿病,但其背后的原因此前却一直不清楚。

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。

这项研究显示了CFTR对胰腺β-细胞功能的一个以前没有被发现的贡献,也为与囊性纤维化相关的糖尿病提供了一个潜在治疗策略。

原文摘要:

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

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