Leptin Modifies the Rat Heart Performance Associated with Mitochondrial Dysfunction Independently of Its Prohypertrophic Effects
Background. Functional receptors for leptin were described on the surface of cardiomyocytes, and there was a prohypertrophic effect with high concentrations of the cytokine. Therefore, leptin could be a link between obesity and the prevalence of cardiovascular diseases. On the other hand, a deleteri...
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| Format: | Article |
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Wiley
2018-01-01
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| Series: | International Journal of Endocrinology |
| Online Access: | http://dx.doi.org/10.1155/2018/6081415 |
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| author | Edna Berzabá-Evoli Cecilia Zazueta Jarumi Hishel Cruz Hernández Nancy Patricia Gómez-Crisóstomo Isela Esther Juárez-Rojop Erick Natividad De la Cruz-Hernández Eduardo Martínez-Abundis |
| author_facet | Edna Berzabá-Evoli Cecilia Zazueta Jarumi Hishel Cruz Hernández Nancy Patricia Gómez-Crisóstomo Isela Esther Juárez-Rojop Erick Natividad De la Cruz-Hernández Eduardo Martínez-Abundis |
| author_sort | Edna Berzabá-Evoli |
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| description | Background. Functional receptors for leptin were described on the surface of cardiomyocytes, and there was a prohypertrophic effect with high concentrations of the cytokine. Therefore, leptin could be a link between obesity and the prevalence of cardiovascular diseases. On the other hand, a deleterious effect of leptin on mitochondrial performance was described, which was also associated with the evolution of cardiac hypertrophy to heart failure. The goal of our study was to analyze the effect of the exposure of rat hearts to a high concentration of leptin on cardiac and mitochondrial function. Methods. Rat hearts were perfused continuously with or without 3.1 nM leptin for 1, 2, 3, or 4 hours. Homogenates and mitochondria were prepared by centrifugation and analyzed for cardiac actin, STAT3, and pSTAT3 by Western blotting, as well as for mitochondrial oxidative phosphorylation, membrane potential, swelling, calcium transport, and content of oxidized lipids. Results. In our results, leptin induced an increased rate-pressure product as a result of increased heart rate and contraction force, as well oxidative stress. In addition, mitochondrial dysfunction expressed as a loss of membrane potential, decreased ability for calcium transport and retention, faster swelling, and less respiratory control was observed. Conclusions. Our results support the role of leptin as a deleterious factor for cardiac function and indicates that mitochondrial dysfunction could be a trigger for cardiac hypertrophy and failure. |
| format | Article |
| id | doaj-art-2c4211deac46498a9816b77a0d884286 |
| institution | Kabale University |
| issn | 1687-8337 1687-8345 |
| language | English |
| publishDate | 2018-01-01 |
| publisher | Wiley |
| record_format | Article |
| series | International Journal of Endocrinology |
| spelling | doaj-art-2c4211deac46498a9816b77a0d8842862025-02-03T05:45:31ZengWileyInternational Journal of Endocrinology1687-83371687-83452018-01-01201810.1155/2018/60814156081415Leptin Modifies the Rat Heart Performance Associated with Mitochondrial Dysfunction Independently of Its Prohypertrophic EffectsEdna Berzabá-Evoli0Cecilia Zazueta1Jarumi Hishel Cruz Hernández2Nancy Patricia Gómez-Crisóstomo3Isela Esther Juárez-Rojop4Erick Natividad De la Cruz-Hernández5Eduardo Martínez-Abundis6Laboratory of Research in Metabolic and Infectious Diseases, Multidisciplinary Academic Division of Comalcalco, Juarez Autonomous University of Tabasco, Villahermosa, TAB, MexicoDepartamento de Biomedicina Cardiovascular, Instituto Nacional de Cardiología (I. Ch.), 14080 Tlalpan, MEX, MexicoLaboratory of Research in Metabolic and Infectious Diseases, Multidisciplinary Academic Division of Comalcalco, Juarez Autonomous University of Tabasco, Villahermosa, TAB, MexicoLaboratory of Research in Metabolic and Infectious Diseases, Multidisciplinary Academic Division of Comalcalco, Juarez Autonomous University of Tabasco, Villahermosa, TAB, MexicoResearch Center, Academic Division of Health Sciences (DACS), Juarez Autonomous University of Tabasco, Villahermosa, TAB, MexicoLaboratory of Research in Metabolic and Infectious Diseases, Multidisciplinary Academic Division of Comalcalco, Juarez Autonomous University of Tabasco, Villahermosa, TAB, MexicoLaboratory of Research in Metabolic and Infectious Diseases, Multidisciplinary Academic Division of Comalcalco, Juarez Autonomous University of Tabasco, Villahermosa, TAB, MexicoBackground. Functional receptors for leptin were described on the surface of cardiomyocytes, and there was a prohypertrophic effect with high concentrations of the cytokine. Therefore, leptin could be a link between obesity and the prevalence of cardiovascular diseases. On the other hand, a deleterious effect of leptin on mitochondrial performance was described, which was also associated with the evolution of cardiac hypertrophy to heart failure. The goal of our study was to analyze the effect of the exposure of rat hearts to a high concentration of leptin on cardiac and mitochondrial function. Methods. Rat hearts were perfused continuously with or without 3.1 nM leptin for 1, 2, 3, or 4 hours. Homogenates and mitochondria were prepared by centrifugation and analyzed for cardiac actin, STAT3, and pSTAT3 by Western blotting, as well as for mitochondrial oxidative phosphorylation, membrane potential, swelling, calcium transport, and content of oxidized lipids. Results. In our results, leptin induced an increased rate-pressure product as a result of increased heart rate and contraction force, as well oxidative stress. In addition, mitochondrial dysfunction expressed as a loss of membrane potential, decreased ability for calcium transport and retention, faster swelling, and less respiratory control was observed. Conclusions. Our results support the role of leptin as a deleterious factor for cardiac function and indicates that mitochondrial dysfunction could be a trigger for cardiac hypertrophy and failure.http://dx.doi.org/10.1155/2018/6081415 |
| spellingShingle | Edna Berzabá-Evoli Cecilia Zazueta Jarumi Hishel Cruz Hernández Nancy Patricia Gómez-Crisóstomo Isela Esther Juárez-Rojop Erick Natividad De la Cruz-Hernández Eduardo Martínez-Abundis Leptin Modifies the Rat Heart Performance Associated with Mitochondrial Dysfunction Independently of Its Prohypertrophic Effects International Journal of Endocrinology |
| title | Leptin Modifies the Rat Heart Performance Associated with Mitochondrial Dysfunction Independently of Its Prohypertrophic Effects |
| title_full | Leptin Modifies the Rat Heart Performance Associated with Mitochondrial Dysfunction Independently of Its Prohypertrophic Effects |
| title_fullStr | Leptin Modifies the Rat Heart Performance Associated with Mitochondrial Dysfunction Independently of Its Prohypertrophic Effects |
| title_full_unstemmed | Leptin Modifies the Rat Heart Performance Associated with Mitochondrial Dysfunction Independently of Its Prohypertrophic Effects |
| title_short | Leptin Modifies the Rat Heart Performance Associated with Mitochondrial Dysfunction Independently of Its Prohypertrophic Effects |
| title_sort | leptin modifies the rat heart performance associated with mitochondrial dysfunction independently of its prohypertrophic effects |
| url | http://dx.doi.org/10.1155/2018/6081415 |
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