通过 BDH1 的酮通量支持骨骼肌和心肌对间歇性限时进食的代谢重塑。

Ashley S Williams, Scott B Crown, Scott P Lyons, Timothy R Koves, Rebecca J Wilson, Jordan M Johnson, Dorothy H Slentz, Daniel P Kelly, Paul A Grimsrud, Guo-Fang Zhang, Deborah M Muoio
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引用次数: 0

摘要

限时进食(TRF)作为一种促进新陈代谢健康的膳食方案已受到人们的关注。本研究对间歇性 TRF(iTRF)计划的健康益处是否需要骨骼肌和心肌中的酮通量提出了质疑。值得注意的是,我们发现β-羟丁酸脱氢酶1(BDH1)独特地富集在来自心脏和红色/氧化骨骼肌的分离线粒体中,而这些肌肉也具有很高的脂肪酸氧化(FAO)能力。利用横纹肌中 BDH1 缺乏的小鼠,我们发现这种酶能优化脂肪酸氧化效率和急性禁食期间的运动耐受性。此外,iTRF 还会导致肌肉组织发生强有力的分子重塑,而肌肉 BDH1 通量确实在赋予这种疗法全面的适应性益处方面发挥了重要作用,包括增加瘦肉质量、线粒体激素生成和丙酮酸代谢重塑。总之,酮通量可增强线粒体生物能,支持 iTRF 诱导的骨骼肌和心脏重塑。
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Ketone flux through BDH1 supports metabolic remodeling of skeletal and cardiac muscles in response to intermittent time-restricted feeding.

Time-restricted feeding (TRF) has gained attention as a dietary regimen that promotes metabolic health. This study questioned if the health benefits of an intermittent TRF (iTRF) schedule require ketone flux specifically in skeletal and cardiac muscles. Notably, we found that the ketolytic enzyme beta-hydroxybutyrate dehydrogenase 1 (BDH1) is uniquely enriched in isolated mitochondria derived from heart and red/oxidative skeletal muscles, which also have high capacity for fatty acid oxidation (FAO). Using mice with BDH1 deficiency in striated muscles, we discover that this enzyme optimizes FAO efficiency and exercise tolerance during acute fasting. Additionally, iTRF leads to robust molecular remodeling of muscle tissues, and muscle BDH1 flux does indeed play an essential role in conferring the full adaptive benefits of this regimen, including increased lean mass, mitochondrial hormesis, and metabolic rerouting of pyruvate. In sum, ketone flux enhances mitochondrial bioenergetics and supports iTRF-induced remodeling of skeletal muscle and heart.

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