Myricetin improves endurance capacity and mitochondrial density by activating SIRT1 and PGC-1α

Abstract Robust mitochondrial respiration provides energy to support physical performance and physiological well-being, whereas mitochondrial malfunction is associated with various pathologies and reduced longevity. In the current study, we tested whether myricetin, a natural flavonol with diverse b...

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Autores principales: Hoe-Yune Jung, Dongyeop Lee, Hye Guk Ryu, Bo-Hwa Choi, Younghoon Go, Namgyu Lee, Dohyun Lee, Heehwa G. Son, Jongsu Jeon, Seong-Hoon Kim, Jong Hyuk Yoon, Seon-Min Park, Seung-Jae V. Lee, In-Kyu Lee, Kwan Yong Choi, Sung Ho Ryu, Kazunari Nohara, Seung-Hee Yoo, Zheng Chen, Kyong-Tai Kim
Formato: article
Lenguaje:EN
Publicado: Nature Portfolio 2017
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Acceso en línea:https://doaj.org/article/10201d00788242438ead92d92999e6dd
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Sumario:Abstract Robust mitochondrial respiration provides energy to support physical performance and physiological well-being, whereas mitochondrial malfunction is associated with various pathologies and reduced longevity. In the current study, we tested whether myricetin, a natural flavonol with diverse biological activities, may impact mitochondrial function and longevity. The mice were orally administered myricetin (50 mg/kg/day) for 3 weeks. Myricetin significantly potentiated aerobic capacity in mice, as evidenced by their increased running time and distance. The elevated mitochondrial function was associated with induction of genes for oxidative phosphorylation and mitochondrial biogenesis in metabolically active tissues. Importantly, myricetin treatment led to decreased PGC-1α acetylation through SIRT1 activation. Furthermore, myricetin significantly improved the healthspan and lifespan of wild-type, but not Sir-2.1-deficient, C. elegans. These results demonstrate that myricetin enhances mitochondrial activity, possibly by activating PGC-1α and SIRT1, to improve physical endurance, strongly suggesting myricetin as a mitochondria-activating agent.