Difference between revisions of "Schleier 2020 J Cardiovasc Transl Res"
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|year=2020 | |year=2020 | ||
|journal=J Cardiovasc Transl Res | |journal=J Cardiovasc Transl Res | ||
|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 | |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 Ca<sup>2+</sup> transients were evaluated at whole heart level. Heart mitochondrial function was evaluated by high-resolution respirometry and H<sub>2</sub>O<sub>2</sub> release. NOD mice presented a reduction in hearth weight. Mitochondrial oxygen fluxes and H<sub>2</sub>O<sub>2</sub> 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 Ca<sup>2+</sup> 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. | ||
|keywords=Arrhythmias, Electrophysiology. Mitochondria. NOD mice, Type 1 diabetes | |keywords=Arrhythmias, Electrophysiology. Mitochondria. NOD mice, Type 1 diabetes | ||
|editor=[[Plangger M]] | |editor=[[Plangger M]] | ||
|mipnetlab=BR Rio de Janeiro Galina A, BR Rio de Janeiro Institute Biomedical Chemistry | |||
}} | }} | ||
{{Labeling | {{Labeling | ||
|area=Respiration | |area=Respiration | ||
|diseases=Diabetes | |||
|organism=Mouse | |||
|tissues=Heart | |||
|preparations=Isolated mitochondria | |||
|couplingstates=LEAK, OXPHOS | |||
|pathways=N, NS, ROX | |||
|instruments=Oxygraph-2k | |instruments=Oxygraph-2k | ||
|additional=2020-06 | |additional=2020-06 | ||
}} | }} |
Revision as of 18:43, 4 June 2020
Schleier Y, Moreno-Loaiza O, López Alarcón MM, Lopes Martins EG, Braga BC, Ramos IP, Galina A, Medei EH (2020) NOD mice recapitulate the cardiac disturbances observed in type 1 diabetes. J Cardiovasc Transl Res [Epub ahead of print]. |
Schleier Y, Moreno-Loaiza O, Lopez Alarcon MM, Lopes Martins EG, Braga BC, Ramos IP, Galina A, Medei EH (2020) J Cardiovasc Transl Res
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. • Keywords: Arrhythmias, Electrophysiology. Mitochondria. NOD mice, Type 1 diabetes • Bioblast editor: Plangger M • O2k-Network Lab: BR Rio de Janeiro Galina A, BR Rio de Janeiro Institute Biomedical Chemistry
Labels: MiParea: Respiration
Pathology: Diabetes
Organism: Mouse Tissue;cell: Heart Preparation: Isolated mitochondria
Coupling state: LEAK, OXPHOS
Pathway: N, NS, ROX
HRR: Oxygraph-2k
2020-06