期刊
JOURNAL OF CARDIOVASCULAR TRANSLATIONAL RESEARCH
卷 14, 期 2, 页码 271-282出版社
SPRINGER
DOI: 10.1007/s12265-020-10039-y
关键词
Type 1 diabetes; Arrhythmias; Mitochondria; NOD mice; Electrophysiology
资金
- Coordenacao de Aperfeicoamento de Pessoal de Nivel Superior (CAPES-PROCAD) [88887.124150/2014-00]
- Brazilian National Research Council (CNPq) [306004/2015-1, 141178/2018-3]
- Carlos Chagas Filho Rio de Janeiro State Research Foundation (FAPERJ) [232724]
- National Institutes of Science and Technology for Regenerative Medicine [573767/2008-4, 465656/2014-5]
- National Institutes of Science and Technology for Biology Structural and Bioimaging
This study found that NOD mice recapitulate cardiac disturbances observed in type 1 diabetes patients, including reduced heart weight, prolonged ECG intervals, and arrhythmias.
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.
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