The Crosstalk between Cardiac Lipotoxicity and Mitochondrial Oxidative Stress in the Cardiac Alterations in Diet-Induced Obesity in Rats
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 n...
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| Format: | Article |
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MDPI AG
2020-02-01
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| Online Access: | https://www.mdpi.com/2073-4409/9/2/451 |
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| author | Sara Jiménez-González Gema Marín-Royo Raquel Jurado-López María Visitación Bartolomé Ana Romero-Miranda María Luaces Fabián Islas María Luisa Nieto Ernesto Martínez-Martínez Victoria Cachofeiro |
| author_facet | Sara Jiménez-González Gema Marín-Royo Raquel Jurado-López María Visitación Bartolomé Ana Romero-Miranda María Luaces Fabián Islas María Luisa Nieto Ernesto Martínez-Martínez Victoria Cachofeiro |
| author_sort | Sara Jiménez-González |
| collection | DOAJ |
| description | 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 <sup>18</sup>-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 |
| first_indexed | 2024-03-12T19:57:06Z |
| format | Article |
| id | doaj.art-8c02ba0dd2e04f4683a640385721142e |
| institution | Directory Open Access Journal |
| issn | 2073-4409 |
| language | English |
| last_indexed | 2024-03-12T19:57:06Z |
| publishDate | 2020-02-01 |
| publisher | MDPI AG |
| record_format | Article |
| series | Cells |
| spelling | doaj.art-8c02ba0dd2e04f4683a640385721142e2023-08-02T02:43:10ZengMDPI AGCells2073-44092020-02-019245110.3390/cells9020451cells9020451The Crosstalk between Cardiac Lipotoxicity and Mitochondrial Oxidative Stress in the Cardiac Alterations in Diet-Induced Obesity in RatsSara Jiménez-González0Gema Marín-Royo1Raquel Jurado-López2María Visitación Bartolomé3Ana Romero-Miranda4María Luaces5Fabián Islas6María Luisa Nieto7Ernesto Martínez-Martínez8Victoria Cachofeiro9Department of Physiology, Instituto de Investigación Sanitaria Gregorio Marañón (IiSGM), School of Medicine, Universidad Complutense, 28040 Madrid, SpainDepartment of Physiology, Instituto de Investigación Sanitaria Gregorio Marañón (IiSGM), School of Medicine, Universidad Complutense, 28040 Madrid, SpainDepartment of Physiology, Instituto de Investigación Sanitaria Gregorio Marañón (IiSGM), School of Medicine, Universidad Complutense, 28040 Madrid, SpainDepartment of Immunology, Ophthalmology and Oto-Rhino-Laringology, Faculty of Psychology, Universidad Complutense, 28223 Madrid, SpainDepartment of Physiology, Instituto de Investigación Sanitaria Gregorio Marañón (IiSGM), School of Medicine, Universidad Complutense, 28040 Madrid, SpainCardiology Department, Cardiovascular Institute, Hospital Clínico San Carlos, 28040 Madrid, SpainCardiology Department, Cardiovascular Institute, Hospital Clínico San Carlos, 28040 Madrid, SpainInstituto de Biología y Genética Molecular, CSIC-Universidad de Valladolid, 47003 Valladolid, SpainDepartment of Physiology, Instituto de Investigación Sanitaria Gregorio Marañón (IiSGM), School of Medicine, Universidad Complutense, 28040 Madrid, SpainDepartment of Physiology, Instituto de Investigación Sanitaria Gregorio Marañón (IiSGM), School of Medicine, Universidad Complutense, 28040 Madrid, SpainThe 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 <sup>18</sup>-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 damagehttps://www.mdpi.com/2073-4409/9/2/451cardiac fibrosiscardiac hypertrophycardiac lipotoxicitymitochondrial functionobesityoxidative stress |
| spellingShingle | Sara Jiménez-González Gema Marín-Royo Raquel Jurado-López María Visitación Bartolomé Ana Romero-Miranda María Luaces Fabián Islas María Luisa Nieto Ernesto Martínez-Martínez Victoria Cachofeiro The Crosstalk between Cardiac Lipotoxicity and Mitochondrial Oxidative Stress in the Cardiac Alterations in Diet-Induced Obesity in Rats Cells cardiac fibrosis cardiac hypertrophy cardiac lipotoxicity mitochondrial function obesity oxidative stress |
| title | The Crosstalk between Cardiac Lipotoxicity and Mitochondrial Oxidative Stress in the Cardiac Alterations in Diet-Induced Obesity in Rats |
| title_full | The Crosstalk between Cardiac Lipotoxicity and Mitochondrial Oxidative Stress in the Cardiac Alterations in Diet-Induced Obesity in Rats |
| title_fullStr | The Crosstalk between Cardiac Lipotoxicity and Mitochondrial Oxidative Stress in the Cardiac Alterations in Diet-Induced Obesity in Rats |
| title_full_unstemmed | The Crosstalk between Cardiac Lipotoxicity and Mitochondrial Oxidative Stress in the Cardiac Alterations in Diet-Induced Obesity in Rats |
| title_short | The Crosstalk between Cardiac Lipotoxicity and Mitochondrial Oxidative Stress in the Cardiac Alterations in Diet-Induced Obesity in Rats |
| title_sort | crosstalk between cardiac lipotoxicity and mitochondrial oxidative stress in the cardiac alterations in diet induced obesity in rats |
| topic | cardiac fibrosis cardiac hypertrophy cardiac lipotoxicity mitochondrial function obesity oxidative stress |
| url | https://www.mdpi.com/2073-4409/9/2/451 |
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