The Crosstalk between Cardiac Lipotoxicity and Mitochondrial Oxidative Stress in the Cardiac Alterations in Diet-Induced Obesity in Rats

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Jiménez-González, Sara and Marín-Royo, Gema and Jurado-López, Raquel and Bartolomé Pascual, Visitación and Romero Miranda, Ana and Luaces Méndez, María and Islas, Fabián and Nieto, María Luisa and Martínez Martínez, Ernesto and Cachofeiro Ramos, Victoria (2020) The Crosstalk between Cardiac Lipotoxicity and Mitochondrial Oxidative Stress in the Cardiac Alterations in Diet-Induced Obesity in Rats. Cells, 9 (2). ISSN 2073-4409

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Official URL: https://www.mdpi.com/2073-4409/9/2/451




Abstract

The impact of the mitochondria-targeted antioxidant MitoQ was evaluated in the cardiac alterations associated with obesity. Male Wistar rats were fed either a high fat diet (HFD, 35% fat) or a standard diet (CT, 3.5% fat) for 7 weeks and treated with MitoQ (200 µM). The effect of MitoQ (5 nM) in rat cardiac myoblasts treated for 24 h with palmitic acid (PA, 200 µM) was evaluated. MitoQ reduced cardiac oxidative stress and prevented the development of cardiac fibrosis, hypertrophy, myocardial 18-FDG uptake reduction, and mitochondrial lipid remodeling in HFD rats. It also ameliorated cardiac mitochondrial protein level changes observed in HFD: reductions in fumarate hydratase, complex I and II, as well as increases in mitofusin 1 (MFN1), peroxisome proliferator-activated receptor gamma coactivator 1-alpha, and cyclophilin F (cycloF). In vitro, MitoQ prevented oxidative stress and ameliorated alterations in mitochondrial proteins observed in palmitic acid (PA)-stimulated cardiac myoblasts: increases in carnitine palmitoyltransferase 1A, cycloF, and cytochrome C. PA induced phosphorylation of extracellular signal-regulated kinases and nuclear factor-κB p65. Therefore, the data show the beneficial effects of MitoQ in the cardiac damage induced by obesity and suggests a crosstalk between lipotoxicity and mitochondrial oxidative stress in this damage.


Item Type:Article
Uncontrolled Keywords:Cardiac fibrosis; cardiac hypertrophy; cardiac lipotoxicity; mitochondrial function; obesity; oxidative stress
Subjects:Medical sciences > Medicine > Cardiology
Medical sciences > Medicine > Physiology
ID Code:61794
Deposited On:06 Aug 2020 11:30
Last Modified:06 Aug 2020 11:30

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