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Coenzyme Q10 protects against burn‐induced mitochondrial dysfunction and impaired insulin signaling in mouse skeletal muscle

Mitochondrial dysfunction is associated with metabolic alterations in various disease states, including major trauma (e.g., burn injury). Metabolic derangements, including muscle insulin resistance and hyperlactatemia, are a clinically significant complication of major trauma. Coenzyme Q10 (CoQ10) i...

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Autores principales: Nakazawa, Harumasa, Ikeda, Kazuhiro, Shinozaki, Shohei, Yasuhara, Shingo, Yu, Yong‐Ming, Martyn, J.A. Jeevendra, Tompkins, Ronald G., Yorozu, Tomoko, Inoue, Satoshi, Kaneki, Masao
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6356165/
https://www.ncbi.nlm.nih.gov/pubmed/30761259
http://dx.doi.org/10.1002/2211-5463.12580
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author Nakazawa, Harumasa
Ikeda, Kazuhiro
Shinozaki, Shohei
Yasuhara, Shingo
Yu, Yong‐Ming
Martyn, J.A. Jeevendra
Tompkins, Ronald G.
Yorozu, Tomoko
Inoue, Satoshi
Kaneki, Masao
author_facet Nakazawa, Harumasa
Ikeda, Kazuhiro
Shinozaki, Shohei
Yasuhara, Shingo
Yu, Yong‐Ming
Martyn, J.A. Jeevendra
Tompkins, Ronald G.
Yorozu, Tomoko
Inoue, Satoshi
Kaneki, Masao
author_sort Nakazawa, Harumasa
collection PubMed
description Mitochondrial dysfunction is associated with metabolic alterations in various disease states, including major trauma (e.g., burn injury). Metabolic derangements, including muscle insulin resistance and hyperlactatemia, are a clinically significant complication of major trauma. Coenzyme Q10 (CoQ10) is an essential cofactor for mitochondrial electron transport, and its reduced form acts as a lipophilic antioxidant. Here, we report that burn injury induces impaired muscle insulin signaling, hyperlactatemia, mitochondrial dysfunction (as indicated by suppressed mitochondrial oxygen consumption rates), morphological alterations of the mitochondria (e. g., enlargement, and loss of cristae structure), mitochondrial oxidative stress, and disruption of mitochondrial integrity (as reflected by increased mitochondrial DNA levels in the cytosol and circulation). All of these alterations were significantly alleviated by CoQ10 treatment compared with vehicle alone. These findings indicate that CoQ10 treatment is efficacious in protecting against mitochondrial dysfunction and insulin resistance in skeletal muscle of burned mice. Our data highlight CoQ10 as a potential new strategy to prevent mitochondrial damage and metabolic dysfunction in burn patients.
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spelling pubmed-63561652019-02-13 Coenzyme Q10 protects against burn‐induced mitochondrial dysfunction and impaired insulin signaling in mouse skeletal muscle Nakazawa, Harumasa Ikeda, Kazuhiro Shinozaki, Shohei Yasuhara, Shingo Yu, Yong‐Ming Martyn, J.A. Jeevendra Tompkins, Ronald G. Yorozu, Tomoko Inoue, Satoshi Kaneki, Masao FEBS Open Bio Research Articles Mitochondrial dysfunction is associated with metabolic alterations in various disease states, including major trauma (e.g., burn injury). Metabolic derangements, including muscle insulin resistance and hyperlactatemia, are a clinically significant complication of major trauma. Coenzyme Q10 (CoQ10) is an essential cofactor for mitochondrial electron transport, and its reduced form acts as a lipophilic antioxidant. Here, we report that burn injury induces impaired muscle insulin signaling, hyperlactatemia, mitochondrial dysfunction (as indicated by suppressed mitochondrial oxygen consumption rates), morphological alterations of the mitochondria (e. g., enlargement, and loss of cristae structure), mitochondrial oxidative stress, and disruption of mitochondrial integrity (as reflected by increased mitochondrial DNA levels in the cytosol and circulation). All of these alterations were significantly alleviated by CoQ10 treatment compared with vehicle alone. These findings indicate that CoQ10 treatment is efficacious in protecting against mitochondrial dysfunction and insulin resistance in skeletal muscle of burned mice. Our data highlight CoQ10 as a potential new strategy to prevent mitochondrial damage and metabolic dysfunction in burn patients. John Wiley and Sons Inc. 2019-01-19 /pmc/articles/PMC6356165/ /pubmed/30761259 http://dx.doi.org/10.1002/2211-5463.12580 Text en © 2018 The Authors. Published by FEBS Press and John Wiley & Sons Ltd. This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
spellingShingle Research Articles
Nakazawa, Harumasa
Ikeda, Kazuhiro
Shinozaki, Shohei
Yasuhara, Shingo
Yu, Yong‐Ming
Martyn, J.A. Jeevendra
Tompkins, Ronald G.
Yorozu, Tomoko
Inoue, Satoshi
Kaneki, Masao
Coenzyme Q10 protects against burn‐induced mitochondrial dysfunction and impaired insulin signaling in mouse skeletal muscle
title Coenzyme Q10 protects against burn‐induced mitochondrial dysfunction and impaired insulin signaling in mouse skeletal muscle
title_full Coenzyme Q10 protects against burn‐induced mitochondrial dysfunction and impaired insulin signaling in mouse skeletal muscle
title_fullStr Coenzyme Q10 protects against burn‐induced mitochondrial dysfunction and impaired insulin signaling in mouse skeletal muscle
title_full_unstemmed Coenzyme Q10 protects against burn‐induced mitochondrial dysfunction and impaired insulin signaling in mouse skeletal muscle
title_short Coenzyme Q10 protects against burn‐induced mitochondrial dysfunction and impaired insulin signaling in mouse skeletal muscle
title_sort coenzyme q10 protects against burn‐induced mitochondrial dysfunction and impaired insulin signaling in mouse skeletal muscle
topic Research Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6356165/
https://www.ncbi.nlm.nih.gov/pubmed/30761259
http://dx.doi.org/10.1002/2211-5463.12580
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