This work aimed at testing the hypothesis that NOD/ShiLtJ mice (NOD) recapitulate the cardiac disturbances observed on type 1 diabetes (T1D). NOD mice were studied 4 weeks after the onset of hyperglycemia, and NOR/Lt mice matched as control. Cardiac function was evaluated by echocardiography and electrocardiography (ECG). Action potentials (AP) and Ca²⁺ transients were evaluated at whole heart level. Heart mitochondrial function was evaluated by high-resolution respirometry and H₂O₂ release. NOD mice presented a reduction in hearth weight. Mitochondrial oxygen fluxes and H₂O₂ release were similar between NOD and NOR mice. ECG revealed a QJ interval prolongation in NOD mice. Furthermore, AP duration at 30% of repolarization was increased, and it depicted slower Ca²⁺ transient kinetics. NOD mice presented greater number/severity of ventricular arrhythmias both in vivo and in vitro. In conclusion, NOD mice evoked cardiac electrical and calcium handling disturbances similar to the observed in T1D.

.

这项工作旨在检验 NOD/ShiLtJ 小鼠 (NOD) 概括了在 1 型糖尿病 (T1D) 上观察到的心脏障碍的假设。在高血糖发作 4 周后研究 NOD 小鼠，并将 NOR/Lt 小鼠匹配为对照。通过超声心动图和心电图（ECG）评估心脏功能。在整个心脏水平评估动作电位 (AP) 和 Ca ²⁺瞬变。通过高分辨率呼​​吸测量法和 H ₂ O ₂释放评估心脏线粒体功能。NOD 小鼠表现出炉膛重量减少。线粒体氧通量和 H ₂ O ₂NOD和NOR小鼠的释放相似。心电图显示 NOD 小鼠的 QJ 间期延长。此外，在 30% 的复极化时 AP 持续时间增加，并且它描绘了较慢的 Ca ²⁺瞬态动力学。NOD 小鼠在体内和体外都表现出更多/严重的室性心律失常。总之，NOD 小鼠诱发了与 T1D 中观察到的类似的心脏电和钙处理障碍。

.