Nutritional Ketosis and Mitohormesis: Potential Implications for Mitochondrial Function and Human Health
Impaired mitochondrial function often results in excessive production of reactive oxygen species (ROS) and is involved in the etiology of many chronic diseases, including cardiovascular disease, diabetes, neurodegenerative disorders, and cancer. Moderate levels of mitochondrial ROS, however, can pro...
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| Format: | Article |
| Language: | English |
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Wiley
2018-01-01
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| Series: | Journal of Nutrition and Metabolism |
| Online Access: | http://dx.doi.org/10.1155/2018/5157645 |
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| author | Vincent J. Miller Frederick A. Villamena Jeff S. Volek |
| author_facet | Vincent J. Miller Frederick A. Villamena Jeff S. Volek |
| author_sort | Vincent J. Miller |
| collection | DOAJ |
| description | Impaired mitochondrial function often results in excessive production of reactive oxygen species (ROS) and is involved in the etiology of many chronic diseases, including cardiovascular disease, diabetes, neurodegenerative disorders, and cancer. Moderate levels of mitochondrial ROS, however, can protect against chronic disease by inducing upregulation of mitochondrial capacity and endogenous antioxidant defense. This phenomenon, referred to as mitohormesis, is induced through increased reliance on mitochondrial respiration, which can occur through diet or exercise. Nutritional ketosis is a safe and physiological metabolic state induced through a ketogenic diet low in carbohydrate and moderate in protein. Such a diet increases reliance on mitochondrial respiration and may, therefore, induce mitohormesis. Furthermore, the ketone β-hydroxybutyrate (BHB), which is elevated during nutritional ketosis to levels no greater than those resulting from fasting, acts as a signaling molecule in addition to its traditionally known role as an energy substrate. BHB signaling induces adaptations similar to mitohormesis, thereby expanding the potential benefit of nutritional ketosis beyond carbohydrate restriction. This review describes the evidence supporting enhancement of mitochondrial function and endogenous antioxidant defense in response to nutritional ketosis, as well as the potential mechanisms leading to these adaptations. |
| format | Article |
| id | doaj-art-b1a9494ec2b24460a396f2fa23342158 |
| institution | Kabale University |
| issn | 2090-0724 2090-0732 |
| language | English |
| publishDate | 2018-01-01 |
| publisher | Wiley |
| record_format | Article |
| series | Journal of Nutrition and Metabolism |
| spelling | doaj-art-b1a9494ec2b24460a396f2fa233421582025-02-03T06:42:14ZengWileyJournal of Nutrition and Metabolism2090-07242090-07322018-01-01201810.1155/2018/51576455157645Nutritional Ketosis and Mitohormesis: Potential Implications for Mitochondrial Function and Human HealthVincent J. Miller0Frederick A. Villamena1Jeff S. Volek2Department of Human Sciences, College of Education and Human Ecology, The Ohio State University, Columbus, OH, USADepartment of Biological Chemistry and Pharmacology, College of Medicine, The Ohio State University, Columbus, OH, USADepartment of Human Sciences, College of Education and Human Ecology, The Ohio State University, Columbus, OH, USAImpaired mitochondrial function often results in excessive production of reactive oxygen species (ROS) and is involved in the etiology of many chronic diseases, including cardiovascular disease, diabetes, neurodegenerative disorders, and cancer. Moderate levels of mitochondrial ROS, however, can protect against chronic disease by inducing upregulation of mitochondrial capacity and endogenous antioxidant defense. This phenomenon, referred to as mitohormesis, is induced through increased reliance on mitochondrial respiration, which can occur through diet or exercise. Nutritional ketosis is a safe and physiological metabolic state induced through a ketogenic diet low in carbohydrate and moderate in protein. Such a diet increases reliance on mitochondrial respiration and may, therefore, induce mitohormesis. Furthermore, the ketone β-hydroxybutyrate (BHB), which is elevated during nutritional ketosis to levels no greater than those resulting from fasting, acts as a signaling molecule in addition to its traditionally known role as an energy substrate. BHB signaling induces adaptations similar to mitohormesis, thereby expanding the potential benefit of nutritional ketosis beyond carbohydrate restriction. This review describes the evidence supporting enhancement of mitochondrial function and endogenous antioxidant defense in response to nutritional ketosis, as well as the potential mechanisms leading to these adaptations.http://dx.doi.org/10.1155/2018/5157645 |
| spellingShingle | Vincent J. Miller Frederick A. Villamena Jeff S. Volek Nutritional Ketosis and Mitohormesis: Potential Implications for Mitochondrial Function and Human Health Journal of Nutrition and Metabolism |
| title | Nutritional Ketosis and Mitohormesis: Potential Implications for Mitochondrial Function and Human Health |
| title_full | Nutritional Ketosis and Mitohormesis: Potential Implications for Mitochondrial Function and Human Health |
| title_fullStr | Nutritional Ketosis and Mitohormesis: Potential Implications for Mitochondrial Function and Human Health |
| title_full_unstemmed | Nutritional Ketosis and Mitohormesis: Potential Implications for Mitochondrial Function and Human Health |
| title_short | Nutritional Ketosis and Mitohormesis: Potential Implications for Mitochondrial Function and Human Health |
| title_sort | nutritional ketosis and mitohormesis potential implications for mitochondrial function and human health |
| url | http://dx.doi.org/10.1155/2018/5157645 |
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