Trimetazidine and exercise provide comparable improvements to high fat diet-induced muscle dysfunction through enhancement of mitochondrial quality control

Abstract Obesity induces skeletal muscle dysfunction. The pathogenesis of which appears to substantially involve mitochondrial dysfunction, arising from impaired quality control. Exercise is a major therapeutic strategy against muscle dysfunction. Trimetazidine, a partial inhibitor of lipid oxidatio...

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Autores principales:	Wenliang Zhang, Baiyang You, Dake Qi, Ling Qiu, Jeffrey W. Ripley-Gonzalez, Fan Zheng, Siqian Fu, Cui Li, Yaoshan Dun, Suixin Liu
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2021
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/e2f80afdf365485b81712d3ac7fe2b10
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spelling	oai:doaj.org-article:e2f80afdf365485b81712d3ac7fe2b102021-12-02T17:37:35ZTrimetazidine and exercise provide comparable improvements to high fat diet-induced muscle dysfunction through enhancement of mitochondrial quality control10.1038/s41598-021-98771-62045-2322https://doaj.org/article/e2f80afdf365485b81712d3ac7fe2b102021-09-01T00:00:00Zhttps://doi.org/10.1038/s41598-021-98771-6https://doaj.org/toc/2045-2322Abstract Obesity induces skeletal muscle dysfunction. The pathogenesis of which appears to substantially involve mitochondrial dysfunction, arising from impaired quality control. Exercise is a major therapeutic strategy against muscle dysfunction. Trimetazidine, a partial inhibitor of lipid oxidation, has been proposed as a metabolic modulator for several cardiovascular pathologies. However, the effects of Trimetazidine on regulating skeletal muscle function are largely unknown. Our present study used cell culture and obese mice models to test a novel hypothesis that Trimetazidine could improve muscle atrophy with similar results to exercise. In C2C12 cells, high palmitic acid-induced atrophy and mitochondrial dysfunction, which could be reversed by the treatment of Trimetazidine. In our animal models, with high-fat diet-induced obesity associated with skeletal muscle atrophy, Trimetazidine prevented muscle dysfunction, corrected metabolic abnormalities, and improved mitochondrial quality control and mitochondrial functions similarly to exercise. Thus, our study suggests that Trimetazidine successfully mimics exercise to enhance mitochondrial quality control leading to improved high-fat diet-induced muscle dysfunction.Wenliang ZhangBaiyang YouDake QiLing QiuJeffrey W. Ripley-GonzalezFan ZhengSiqian FuCui LiYaoshan DunSuixin LiuNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 11, Iss 1, Pp 1-12 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Wenliang Zhang Baiyang You Dake Qi Ling Qiu Jeffrey W. Ripley-Gonzalez Fan Zheng Siqian Fu Cui Li Yaoshan Dun Suixin Liu Trimetazidine and exercise provide comparable improvements to high fat diet-induced muscle dysfunction through enhancement of mitochondrial quality control
description	Abstract Obesity induces skeletal muscle dysfunction. The pathogenesis of which appears to substantially involve mitochondrial dysfunction, arising from impaired quality control. Exercise is a major therapeutic strategy against muscle dysfunction. Trimetazidine, a partial inhibitor of lipid oxidation, has been proposed as a metabolic modulator for several cardiovascular pathologies. However, the effects of Trimetazidine on regulating skeletal muscle function are largely unknown. Our present study used cell culture and obese mice models to test a novel hypothesis that Trimetazidine could improve muscle atrophy with similar results to exercise. In C2C12 cells, high palmitic acid-induced atrophy and mitochondrial dysfunction, which could be reversed by the treatment of Trimetazidine. In our animal models, with high-fat diet-induced obesity associated with skeletal muscle atrophy, Trimetazidine prevented muscle dysfunction, corrected metabolic abnormalities, and improved mitochondrial quality control and mitochondrial functions similarly to exercise. Thus, our study suggests that Trimetazidine successfully mimics exercise to enhance mitochondrial quality control leading to improved high-fat diet-induced muscle dysfunction.
format	article
author	Wenliang Zhang Baiyang You Dake Qi Ling Qiu Jeffrey W. Ripley-Gonzalez Fan Zheng Siqian Fu Cui Li Yaoshan Dun Suixin Liu
author_facet	Wenliang Zhang Baiyang You Dake Qi Ling Qiu Jeffrey W. Ripley-Gonzalez Fan Zheng Siqian Fu Cui Li Yaoshan Dun Suixin Liu
author_sort	Wenliang Zhang
title	Trimetazidine and exercise provide comparable improvements to high fat diet-induced muscle dysfunction through enhancement of mitochondrial quality control
title_short	Trimetazidine and exercise provide comparable improvements to high fat diet-induced muscle dysfunction through enhancement of mitochondrial quality control
title_full	Trimetazidine and exercise provide comparable improvements to high fat diet-induced muscle dysfunction through enhancement of mitochondrial quality control
title_fullStr	Trimetazidine and exercise provide comparable improvements to high fat diet-induced muscle dysfunction through enhancement of mitochondrial quality control
title_full_unstemmed	Trimetazidine and exercise provide comparable improvements to high fat diet-induced muscle dysfunction through enhancement of mitochondrial quality control
title_sort	trimetazidine and exercise provide comparable improvements to high fat diet-induced muscle dysfunction through enhancement of mitochondrial quality control
publisher	Nature Portfolio
publishDate	2021
url	https://doaj.org/article/e2f80afdf365485b81712d3ac7fe2b10
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Trimetazidine and exercise provide comparable improvements to high fat diet-induced muscle dysfunction through enhancement of mitochondrial quality control

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