Zhang Jie, Chen Bo, Zou Ke
Department of Police Physical Training, Zhejiang Police Collage, Zhejiang, China.
Department of Physical Education, Beijing University of Chemical Technology, 15 North Third Ring East Road, Chaoyang District, Beijing, 100029, China.
Open Life Sci. 2023 Feb 23;18(1):20220570. doi: 10.1515/biol-2022-0570. eCollection 2023.
Ketogenic diet (KD) has been proven to be an optional avenue in weight control. However, the impacts of KD on muscle strength and exercise endurance remain unclear. In this study, mice were randomly allocated to normal diet and KD groups to assess their exercise tolerance and transcriptomic changes of the gastrocnemius. KD suppressed body-weight and glucose levels and augmented blood ketone levels of mice. The total cholesterol, free fatty acids, and β-hydroxybutyric acid levels were higher and triglycerides and aspartate aminotransferase levels were lower in KD group. There was no notable difference in running distance/time and weight-bearing swimming time between the two groups. Furthermore, KD alleviated the protein levels of PGC-1α, p62, TnI FS, p-AMPKα, and p-Smad3, while advancing the LC3 II and TnI SS protein levels in the gastrocnemius tissues. RNA-sequencing found that 387 differentially expressed genes were filtered, and Cpt1b, Acadl, Eci2, Mlycd, Pdk4, Ptprc, C1qa, Emr1, Fcgr3, and Ctss were considered to be the hub genes. Our findings suggest that KD effectively reduced body weight but did not affect skeletal muscle strength and exercise endurance via AMPK/PGC-1α, Smad3, and p62/LC3 signaling pathways and these hub genes could be potential targets for muscle function in KD-treated mice.
生酮饮食（KD）已被证明是控制体重的一种可选方法。然而，KD对肌肉力量和运动耐力的影响仍不明确。在本研究中，将小鼠随机分为正常饮食组和KD组，以评估它们的运动耐力以及腓肠肌的转录组变化。KD抑制了小鼠的体重和血糖水平，并提高了血液中的酮水平。KD组的总胆固醇、游离脂肪酸和β-羟基丁酸水平较高，而甘油三酯和天冬氨酸转氨酶水平较低。两组之间的跑步距离/时间和负重游泳时间没有显著差异。此外，KD降低了腓肠肌组织中PGC-1α、p62、TnI FS、p-AMPKα和p-Smad3的蛋白水平，同时提高了LC3 II和TnI SS的蛋白水平。RNA测序发现筛选出了387个差异表达基因，Cpt1b、Acadl、Eci2、Mlycd、Pdk4、Ptprc、C1qa、Emr1、Fcgr3和Ctss被认为是关键基因。我们的研究结果表明，KD有效地减轻了体重，但未通过AMPK/PGC-1α、Smad3和p62/LC3信号通路影响骨骼肌力量和运动耐力，并且这些关键基因可能是KD处理小鼠肌肉功能的潜在靶点。
