Ketone Bodies and Cardiovascular Disease: An Alternate Fuel Source to the Rescue
The increased metabolic activity of the heart as a pump involves a high demand of mitochondrial adenosine triphosphate (ATP) production for its mechanical and electrical activities accomplished mainly via oxidative phosphorylation, supplying up to 95% of the necessary ATP production, with the rest a...
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| Format: | Article |
| Language: | English |
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MDPI AG
2023-02-01
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| Series: | International Journal of Molecular Sciences |
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| Online Access: | https://www.mdpi.com/1422-0067/24/4/3534 |
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| author | Antonis S. Manolis Theodora A. Manolis Antonis A. Manolis |
| author_facet | Antonis S. Manolis Theodora A. Manolis Antonis A. Manolis |
| author_sort | Antonis S. Manolis |
| collection | DOAJ |
| description | The increased metabolic activity of the heart as a pump involves a high demand of mitochondrial adenosine triphosphate (ATP) production for its mechanical and electrical activities accomplished mainly via oxidative phosphorylation, supplying up to 95% of the necessary ATP production, with the rest attained by substrate-level phosphorylation in glycolysis. In the normal human heart, fatty acids provide the principal fuel (40–70%) for ATP generation, followed mainly by glucose (20–30%), and to a lesser degree (<5%) by other substrates (lactate, ketones, pyruvate and amino acids). Although ketones contribute 4–15% under normal situations, the rate of glucose use is drastically diminished in the hypertrophied and failing heart which switches to ketone bodies as an alternate fuel which are oxidized in lieu of glucose, and if adequately abundant, they reduce myocardial fat delivery and usage. Increasing cardiac ketone body oxidation appears beneficial in the context of heart failure (HF) and other pathological cardiovascular (CV) conditions. Also, an enhanced expression of genes crucial for ketone break down facilitates fat or ketone usage which averts or slows down HF, potentially by avoiding the use of glucose-derived carbon needed for anabolic processes. These issues of ketone body utilization in HF and other CV diseases are herein reviewed and pictorially illustrated. |
| first_indexed | 2024-03-11T08:42:45Z |
| format | Article |
| id | doaj.art-37c7e632761d47ceb5cff74d9cbaf339 |
| institution | Directory Open Access Journal |
| issn | 1661-6596 1422-0067 |
| language | English |
| last_indexed | 2024-03-11T08:42:45Z |
| publishDate | 2023-02-01 |
| publisher | MDPI AG |
| record_format | Article |
| series | International Journal of Molecular Sciences |
| spelling | doaj.art-37c7e632761d47ceb5cff74d9cbaf3392023-11-16T21:01:24ZengMDPI AGInternational Journal of Molecular Sciences1661-65961422-00672023-02-01244353410.3390/ijms24043534Ketone Bodies and Cardiovascular Disease: An Alternate Fuel Source to the RescueAntonis S. Manolis0Theodora A. Manolis1Antonis A. Manolis2School of Medicine, Athens University, 115 27 Athens, GreeceSchool of Medicine, Athens University, 115 27 Athens, GreeceSchool of Medicine, Patras University, 265 04 Patras, GreeceThe increased metabolic activity of the heart as a pump involves a high demand of mitochondrial adenosine triphosphate (ATP) production for its mechanical and electrical activities accomplished mainly via oxidative phosphorylation, supplying up to 95% of the necessary ATP production, with the rest attained by substrate-level phosphorylation in glycolysis. In the normal human heart, fatty acids provide the principal fuel (40–70%) for ATP generation, followed mainly by glucose (20–30%), and to a lesser degree (<5%) by other substrates (lactate, ketones, pyruvate and amino acids). Although ketones contribute 4–15% under normal situations, the rate of glucose use is drastically diminished in the hypertrophied and failing heart which switches to ketone bodies as an alternate fuel which are oxidized in lieu of glucose, and if adequately abundant, they reduce myocardial fat delivery and usage. Increasing cardiac ketone body oxidation appears beneficial in the context of heart failure (HF) and other pathological cardiovascular (CV) conditions. Also, an enhanced expression of genes crucial for ketone break down facilitates fat or ketone usage which averts or slows down HF, potentially by avoiding the use of glucose-derived carbon needed for anabolic processes. These issues of ketone body utilization in HF and other CV diseases are herein reviewed and pictorially illustrated.https://www.mdpi.com/1422-0067/24/4/3534ketone bodiesbeta-hydroxybutyrateacetoacetateacetonecardiovascular diseaseheart failure |
| spellingShingle | Antonis S. Manolis Theodora A. Manolis Antonis A. Manolis Ketone Bodies and Cardiovascular Disease: An Alternate Fuel Source to the Rescue International Journal of Molecular Sciences ketone bodies beta-hydroxybutyrate acetoacetate acetone cardiovascular disease heart failure |
| title | Ketone Bodies and Cardiovascular Disease: An Alternate Fuel Source to the Rescue |
| title_full | Ketone Bodies and Cardiovascular Disease: An Alternate Fuel Source to the Rescue |
| title_fullStr | Ketone Bodies and Cardiovascular Disease: An Alternate Fuel Source to the Rescue |
| title_full_unstemmed | Ketone Bodies and Cardiovascular Disease: An Alternate Fuel Source to the Rescue |
| title_short | Ketone Bodies and Cardiovascular Disease: An Alternate Fuel Source to the Rescue |
| title_sort | ketone bodies and cardiovascular disease an alternate fuel source to the rescue |
| topic | ketone bodies beta-hydroxybutyrate acetoacetate acetone cardiovascular disease heart failure |
| url | https://www.mdpi.com/1422-0067/24/4/3534 |
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