Melatonin Alleviates Liver Mitochondrial Dysfunction in Leptin-Deficient Mice
Despite efforts to elucidate the cellular adaptations induced by obesity, cellular bioenergetics is currently considered a crucial target. New strategies to delay the onset of the hazardous adaptations induced by obesity are needed. Therefore, we evaluated the effects of 4 weeks of melatonin treatme...
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| Veröffentlicht in: | International journal of molecular sciences 2024-08, Vol.25 (16), p.8677 |
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| creator | de Luxán-Delgado, Beatriz Potes, Yaiza Rubio-González, Adrian Solano, Juan José Boga, José Antonio Antuña, Eduardo Cachán-Vega, Cristina Bermejo-Millo, Juan Carlos Menéndez-Coto, Nerea García-González, Claudia Pereira, Gonçalo C Caballero, Beatriz Coto-Montes, Ana Vega-Naredo, Ignacio |
| description | Despite efforts to elucidate the cellular adaptations induced by obesity, cellular bioenergetics is currently considered a crucial target. New strategies to delay the onset of the hazardous adaptations induced by obesity are needed. Therefore, we evaluated the effects of 4 weeks of melatonin treatment on mitochondrial function and lipid metabolism in the livers of leptin-deficient mice. Our results revealed that the absence of leptin increased lipid storage in the liver and induced significant mitochondrial alterations, which were ultimately responsible for defective ATP production and reactive oxygen species overproduction. Moreover, leptin deficiency promoted mitochondrial biogenesis, fusion, and outer membrane permeabilization. Melatonin treatment reduced the bioenergetic deficit found in ob/ob mice, alleviating some mitochondrial alterations in the electron transport chain machinery, biogenesis, dynamics, respiration, ATP production, and mitochondrial outer membrane permeabilization. Given the role of melatonin in maintaining mitochondrial homeostasis, it could be used as a therapeutic agent against adipogenic steatosis. |
| doi_str_mv | 10.3390/ijms25168677 |
| format | Article |
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New strategies to delay the onset of the hazardous adaptations induced by obesity are needed. Therefore, we evaluated the effects of 4 weeks of melatonin treatment on mitochondrial function and lipid metabolism in the livers of leptin-deficient mice. Our results revealed that the absence of leptin increased lipid storage in the liver and induced significant mitochondrial alterations, which were ultimately responsible for defective ATP production and reactive oxygen species overproduction. Moreover, leptin deficiency promoted mitochondrial biogenesis, fusion, and outer membrane permeabilization. Melatonin treatment reduced the bioenergetic deficit found in ob/ob mice, alleviating some mitochondrial alterations in the electron transport chain machinery, biogenesis, dynamics, respiration, ATP production, and mitochondrial outer membrane permeabilization. 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Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). 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New strategies to delay the onset of the hazardous adaptations induced by obesity are needed. Therefore, we evaluated the effects of 4 weeks of melatonin treatment on mitochondrial function and lipid metabolism in the livers of leptin-deficient mice. Our results revealed that the absence of leptin increased lipid storage in the liver and induced significant mitochondrial alterations, which were ultimately responsible for defective ATP production and reactive oxygen species overproduction. Moreover, leptin deficiency promoted mitochondrial biogenesis, fusion, and outer membrane permeabilization. Melatonin treatment reduced the bioenergetic deficit found in ob/ob mice, alleviating some mitochondrial alterations in the electron transport chain machinery, biogenesis, dynamics, respiration, ATP production, and mitochondrial outer membrane permeabilization. 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| ispartof | International journal of molecular sciences, 2024-08, Vol.25 (16), p.8677 |
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| source | MDPI - Multidisciplinary Digital Publishing Institute; MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; PubMed Central |
| subjects | Adenosine Triphosphate - metabolism Animals Biosynthesis Body fat Circadian rhythm Cytochrome Dehydrogenases Diabetes Energy Metabolism - drug effects Glucose Homeostasis Insulin resistance Leptin - deficiency Leptin - metabolism Lipid Metabolism - drug effects Lipids Liver Liver - drug effects Liver - metabolism Male Melatonin Melatonin - pharmacology Metabolism Mice Mice, Inbred C57BL Mice, Knockout Mitochondria Mitochondria, Liver - drug effects Mitochondria, Liver - metabolism Mitochondrial DNA Obesity Obesity - drug therapy Obesity - metabolism Oxidation Proteins Reactive oxygen species Reactive Oxygen Species - metabolism Respiration Weight control |
| title | Melatonin Alleviates Liver Mitochondrial Dysfunction in Leptin-Deficient Mice |
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