糖尿病心肌病（DCM）患者的心电图出现心律失常相关的QT间期延长。心肌电生理的研究显示，糖尿病动物模型心肌细胞电生理发生重构，其中包括Iks下调。Iks通道由KCNQ1编码的构成孔区的α亚单位和KCNE1编码的β亚单位构成。KCNQ1和/或KCNE1的基因突变引起QT间期延长。Iks功能变化是心律失常发生的基础之一。胰岛素是一个多效性激素，研究显示高胰岛素血症会引发QT间期延长，QT间期延长主要是由于心肌细胞动作电位复极减慢，然而对胰岛素是否直接调控心肌离子通道的了解甚少。因此，本课题拟在培养成年健康豚鼠单个心室肌细胞上观察胰岛素对Iks的直接作用及其机制。本研究将对阐明糖尿病心肌电生理重构的机制具有重要的意义，以及为临床合理应用胰岛素提供科学基础；同时也将为防治心律失常的发生提供新的干预靶点。

Prolonged QT interval were observed in patients with diabetic cardiomyopathy (DCM), which has become a clinical problem because it increases the risk of lethal ventrical arrhythmia. In animal model of type I diabeties mellitus, myocardial electrophysiological studies have shown that diabetic cardiomyocytes are electrophysiological remodeling, which includes the slowly activating delayed rectifier potassium currents (Iks) down-regulation. The Iks channel is composed of KCNQ1 and KCNE1 subunits, whose gene mutations cause prolongation of QT interval. Iks is the one of the basics ion currents of arrhythmia. Insulin is a pleiotropic hormone, studies have shown that hyperinsulinemia are associated with QT prolongation. Prolonged QT interval is mainly due to delay the action potential repolarization,but little is known about whether insulin directly regulates cardiac ion channels at present.Therefore, The current study was designed to observe the direct effects of insulin on Iks and its mechanism in the culture adult healthy guinea pig single ventricular myocytes. This study will play an important role in elucidating the mechanism of electrophysiological remodeling in DCM and provide a scientific basis for the rational application of insulin in clinical practice; it will also provide a new target for the prevention and treatment of arrhythmia.