| Literature DB >> 32468298 |
Ygor Schleier1, Oscar Moreno-Loaiza1, Maria Micaela López Alarcón1, Eduarda Gabrielle Lopes Martins1,2, Bruno Cabral Braga1, Isalira Peroba Ramos3, Antonio Galina2, Emiliano Horacio Medei4,5,6.
Abstract
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. Graphical Abstract .Entities:
Keywords: Arrhythmias; Electrophysiology; Mitochondria; NOD mice; Type 1 diabetes
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Year: 2020 PMID: 32468298 DOI: 10.1007/s12265-020-10039-y
Source DB: PubMed Journal: J Cardiovasc Transl Res ISSN: 1937-5387 Impact factor: 4.132