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N-acetyltaurine and Acetylcarnitine Production for the Mitochondrial Acetyl-CoA Regulation in Skeletal Muscles during Endurance Exercises

During endurance exercises, a large amount of mitochondrial acetyl-CoA is produced in skeletal muscles from lipids, and the excess acetyl-CoA suppresses the metabolic flux from glycolysis to the TCA cycle. This study evaluated the hypothesis that taurine and carnitine act as a buffer of the acetyl m...

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Autores principales: Miyazaki, Teruo, Nakamura-Shinya, Yuho, Ebina, Kei, Komine, Shoichi, Ra, Song-Gyu, Ishikura, Keisuke, Ohmori, Hajime, Honda, Akira
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8401229/
https://www.ncbi.nlm.nih.gov/pubmed/34436463
http://dx.doi.org/10.3390/metabo11080522
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author Miyazaki, Teruo
Nakamura-Shinya, Yuho
Ebina, Kei
Komine, Shoichi
Ra, Song-Gyu
Ishikura, Keisuke
Ohmori, Hajime
Honda, Akira
author_facet Miyazaki, Teruo
Nakamura-Shinya, Yuho
Ebina, Kei
Komine, Shoichi
Ra, Song-Gyu
Ishikura, Keisuke
Ohmori, Hajime
Honda, Akira
author_sort Miyazaki, Teruo
collection PubMed
description During endurance exercises, a large amount of mitochondrial acetyl-CoA is produced in skeletal muscles from lipids, and the excess acetyl-CoA suppresses the metabolic flux from glycolysis to the TCA cycle. This study evaluated the hypothesis that taurine and carnitine act as a buffer of the acetyl moiety of mitochondrial acetyl-CoA derived from the short- and long-chain fatty acids of skeletal muscles during endurance exercises. In human subjects, the serum concentrations of acetylated forms of taurine (NAT) and carnitine (ACT), which are the metabolites of acetyl-CoA buffering, significantly increased after a full marathon. In the culture medium of primary human skeletal muscle cells, NAT and ACT concentrations significantly increased when they were cultured with taurine and acetate or with carnitine and palmitic acid, respectively. The increase in the mitochondrial acetyl-CoA/free CoA ratio induced by acetate and palmitic acid was suppressed by taurine and carnitine, respectively. Elevations of NAT and ACT in the blood of humans during endurance exercises might serve the buffering of the acetyl-moiety in mitochondria by taurine and carnitine, respectively. The results suggest that blood levels of NAT and ACT indicate energy production status from fatty acids in the skeletal muscles of humans undergoing endurance exercise.
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spelling pubmed-84012292021-08-29 N-acetyltaurine and Acetylcarnitine Production for the Mitochondrial Acetyl-CoA Regulation in Skeletal Muscles during Endurance Exercises Miyazaki, Teruo Nakamura-Shinya, Yuho Ebina, Kei Komine, Shoichi Ra, Song-Gyu Ishikura, Keisuke Ohmori, Hajime Honda, Akira Metabolites Article During endurance exercises, a large amount of mitochondrial acetyl-CoA is produced in skeletal muscles from lipids, and the excess acetyl-CoA suppresses the metabolic flux from glycolysis to the TCA cycle. This study evaluated the hypothesis that taurine and carnitine act as a buffer of the acetyl moiety of mitochondrial acetyl-CoA derived from the short- and long-chain fatty acids of skeletal muscles during endurance exercises. In human subjects, the serum concentrations of acetylated forms of taurine (NAT) and carnitine (ACT), which are the metabolites of acetyl-CoA buffering, significantly increased after a full marathon. In the culture medium of primary human skeletal muscle cells, NAT and ACT concentrations significantly increased when they were cultured with taurine and acetate or with carnitine and palmitic acid, respectively. The increase in the mitochondrial acetyl-CoA/free CoA ratio induced by acetate and palmitic acid was suppressed by taurine and carnitine, respectively. Elevations of NAT and ACT in the blood of humans during endurance exercises might serve the buffering of the acetyl-moiety in mitochondria by taurine and carnitine, respectively. The results suggest that blood levels of NAT and ACT indicate energy production status from fatty acids in the skeletal muscles of humans undergoing endurance exercise. MDPI 2021-08-06 /pmc/articles/PMC8401229/ /pubmed/34436463 http://dx.doi.org/10.3390/metabo11080522 Text en © 2021 by the authors. https://creativecommons.org/licenses/by/4.0/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/).
spellingShingle Article
Miyazaki, Teruo
Nakamura-Shinya, Yuho
Ebina, Kei
Komine, Shoichi
Ra, Song-Gyu
Ishikura, Keisuke
Ohmori, Hajime
Honda, Akira
N-acetyltaurine and Acetylcarnitine Production for the Mitochondrial Acetyl-CoA Regulation in Skeletal Muscles during Endurance Exercises
title N-acetyltaurine and Acetylcarnitine Production for the Mitochondrial Acetyl-CoA Regulation in Skeletal Muscles during Endurance Exercises
title_full N-acetyltaurine and Acetylcarnitine Production for the Mitochondrial Acetyl-CoA Regulation in Skeletal Muscles during Endurance Exercises
title_fullStr N-acetyltaurine and Acetylcarnitine Production for the Mitochondrial Acetyl-CoA Regulation in Skeletal Muscles during Endurance Exercises
title_full_unstemmed N-acetyltaurine and Acetylcarnitine Production for the Mitochondrial Acetyl-CoA Regulation in Skeletal Muscles during Endurance Exercises
title_short N-acetyltaurine and Acetylcarnitine Production for the Mitochondrial Acetyl-CoA Regulation in Skeletal Muscles during Endurance Exercises
title_sort n-acetyltaurine and acetylcarnitine production for the mitochondrial acetyl-coa regulation in skeletal muscles during endurance exercises
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8401229/
https://www.ncbi.nlm.nih.gov/pubmed/34436463
http://dx.doi.org/10.3390/metabo11080522
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