Title: Voltage-gated K+ channel KCNQ1 regulates insulin secretion in MIN6 β-cell line.

Authors: Kazuya Yamagata, Takafumi Senokuchi, Meihong Lu, Makoto Takemoto, Md Fazlul Karim, Chisa Go, Yoshifumi Sato, Mitsutoki Hatta, Tatsuya Yoshizawa, Eiichi Araki, Junichi Miyazaki, Wen-Jie Song

Journal, date & volume: Biochem. Biophys. Res. Commun., 2011 Apr 15 , 407, 620-5

PubMed link: http://www.ncbi.nlm.nih.gov/pubmed/21426901

Abstract
KCNQ1, located on 11p15.5, encodes a voltage-gated K(+) channel with six transmembrane regions, and loss-of-function mutations in the KCNQ1 gene cause hereditary long QT syndrome. Recent genetic studies have identified that single nucleotide polymorphisms located in intron 15 of the KCNQ1 gene are strongly associated with type 2 diabetes and impaired insulin secretion. In order to understand the role of KCNQ1 in insulin secretion, we introduced KCNQ1 into the MIN6 mouse β-cell line using a retrovirus-mediated gene transfer system. In KCNQ1 transferred MIN6 cells, both the density of the KCNQ1 current and the density of the total K(+) current were significantly increased. In addition, insulin secretion by glucose, pyruvate, or tolbutamide was significantly impaired by KCNQ1-overexpressing MIN6 cells. These results suggest that increased KCNQ1 protein expression limits insulin secretion from pancreatic β-cells by regulating the potassium channel current.