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首页> 外文期刊>Journal of cellular physiology. >Insulin acts as an atypical KCNQ1/KCNE1‐current activator and reverses long QT in insulin‐resistant aged rats by accelerating the ventricular action potential repolarization through affecting the β3‐adrenergic receptor signaling pathway
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Insulin acts as an atypical KCNQ1/KCNE1‐current activator and reverses long QT in insulin‐resistant aged rats by accelerating the ventricular action potential repolarization through affecting the β3‐adrenergic receptor signaling pathway

机译：胰岛素作为一个典型的KCNQ1 / KCNE1电流激活和逆转QT间期延长通过加快老龄大鼠抗胰岛素量心室动作电位复极化通过影响β3肾上腺素能受体信号通路

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Abstract Insufficient‐heart function is associated with myocardial insulin resistance in the elderly, particularly?associated with long‐QT, in a dependency on dysfunctional KCNQ1/KCNE1‐channels. So, we aimed to examine the contribution of alterations in KCNQ1/KCNE1‐current (IKs) to the aging‐related remodeling of the heart as well as the role of insulin treatment on IKs in the aged rats. Prolonged late‐phase action potential (AP) repolarization of ventricular cardiomyocytes from insulin‐resistant 24‐month‐old rats was significantly reversed by in vitro treatment of insulin or PKG inhibitor (in vivo, as well) via recovery in depressed IKs. Although the protein level of either KCNQ1 or KCNE1 in cardiomyocytes was not affected with aging, PKG level was significantly increased in those cells. The inhibited IKs in β3‐ARs‐stimulated cells could be reversed with a PKG inhibitor, indicating the correlation between PKG‐activation and β3‐ARs activation. Furthermore, in vivo treatment of aged rats, characterized by β3‐ARs activation, with either insulin or a PKG inhibitor for 2 weeks provided significant recoveries in IKs, prolonged late phases of APs, prolonged QT‐intervals, and low heart rates without no effect on insulin resistance. In vivo insulin treatment provided also significant recovery in increased PKG and decreased PIP2 level, without the insulin effect on the KCNQ1 level in β3‐ARs overexpressed cells. The inhibition of IKs in aged‐rat cardiomyocytes seems to be associated with activated β3‐ARs dependent remodeling in the interaction between KCNQ1 and KCNE1. Significant recoveries in ventricular‐repolarization of insulin‐treated aged cardiomyocytes via recovery in IKs strongly emphasize two important issues: (1) IKs can be a novel target in aging‐associated remodeling in the heart and insulin may be a cardioprotective agent in the maintenance of normal heart function during the aging process. (2) This study is one of the first to demonstrate insulin's?benefits on long‐QT in insulin‐resistant aged rats by accelerating the ventricular AP repolarization through reversing the depressed IKs via affecting the β3‐ARs signaling pathway and particularly affecting activated PKG.
机译：文摘所致心脏功能不足有关与心肌胰岛素抵抗老年人,特别是吗?依赖于功能失调KCNQ1 / KCNE1必经通道。变化的贡献KCNQ1 / KCNE1检测电流(IKs次方)老化相关心脏重塑的作用胰岛素治疗在老年大鼠IKs次方。长时间的必经阶段后期动作电位(AP)心室复极化的心肌细胞抗胰岛素量24月应承担的老老鼠通过体外治疗显著逆转胰岛素或包裹抑制剂(体内)通过复苏沮丧IKs次方。心肌细胞的KCNQ1或KCNE1水平不影响与衰老,包裹级别是什么在这些细胞显著增加。抑制β3 IKs次方ARs应承担的刺激细胞可以与PKG抑制剂逆转,表明相关性PKG的激活和β3农业研究所激活。老老鼠,特点是β3 ARs应承担的激活,与胰岛素或PKG为2抑制剂周提供显著复苏IKs次方,长时间的APs的后期阶段,延长了QT间隔,应承担和低心率没有没有对胰岛素抵抗的影响。治疗也提供显著复苏增加包裹和减少PIP2水平,没有胰岛素影响β3 ARs应承担KCNQ1水平过表达细胞。年龄所致大鼠心肌细胞似乎是相关联的激活β3农业研究所依赖的重构KCNQ1和KCNE1之间的互动。复苏在心室复极化等胰岛素治疗老年心肌细胞通过复苏在IKs次方强烈强调两个重要问题:(1) IKs次方可以在老化的一种新颖的目标相关心和胰岛素可能重塑心血管代理的维护在老化过程中正常的心脏功能。(2)本研究是首次证明之一胰岛素的吗?通过加快老龄大鼠抗胰岛素量通过逆转心室美联社复极化通过影响抑郁IKs次方β3农业研究所信号通路,特别是影响激活包裹。

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