Liu Jun, Lou Shu-Jie
School of Exercise and Health, Shanghai University of Sport, Shanghai 200438, China.
Sheng Li Xue Bao. 2024 Apr 25;76(2):224-232.
The present study aims to investigate the production of ketone body in the liver of mice after 6 weeks of high-intensity interval training (HIIT) intervention and explore the possible mechanisms. Male C57BL/6J mice (7-week-old) were randomly divided into control and HIIT groups. The control group did not engage in exercise, while the HIIT group underwent a 6-week HIIT (10° slope treadmill exercise). Changes in weight and body composition were recorded, and blood ketone body levels were measured before, immediately after, and 1 h after each HIIT exercise. After 6-week HIIT, the levels of free fatty acids in the liver and serum were detected using reagent kits, and expression levels of regulatory factors and key enzymes of ketone body production in the mouse liver were detected by Western blot and qPCR. The results showed that, the blood ketone body levels in the HIIT group significantly increased immediately after a single HIIT and 1 h after HIIT, compared with that before HIIT. The body weight of the control group gradually increased within 6 weeks, while the HIIT group mice did not show significant weight gain. After 6-week HIIT, compared with the control group, the HIIT group showed decreased body fat ratio, increased lean body weight ratio, and increased free fatty acid levels in liver and serum. Liver carnitine palmitoyl transferase-I (CPT-I), peroxisome proliferator activated receptor α (PPARα), and fibroblast growth factor 21 (FGF21) protein expression levels were up-regulated, whereas mammalian target of rapamycin complex 1 (mTORC1) protein expression level was significantly down-regulated in the HIIT group, compared with those in the control group. These results suggest that HIIT induces hepatic ketone body production through altering mTORC1, PPARα and FGF21 expression in mice.
本研究旨在探讨高强度间歇训练（HIIT）干预6周后小鼠肝脏中酮体的产生情况，并探索其可能的机制。将7周龄的雄性C57BL/6J小鼠随机分为对照组和HIIT组。对照组不进行运动，而HIIT组进行为期6周的HIIT（10°坡度跑步机运动）。记录体重和身体成分的变化，并在每次HIIT运动前、运动后即刻和运动后1小时测量血酮体水平。HIIT干预6周后，使用试剂盒检测肝脏和血清中游离脂肪酸水平，并通过蛋白质免疫印迹法（Western blot）和实时荧光定量聚合酶链反应（qPCR）检测小鼠肝脏中酮体生成调节因子和关键酶的表达水平。结果显示，与HIIT运动前相比，HIIT组单次运动后即刻及运动后1小时血酮体水平显著升高。对照组体重在6周内逐渐增加，而HIIT组小鼠体重未显著增加。HIIT干预6周后，与对照组相比，HIIT组体脂率降低，瘦体重率增加，肝脏和血清中游离脂肪酸水平升高。与对照组相比，HIIT组肝脏肉碱棕榈酰转移酶-I（CPT-I）、过氧化物酶体增殖物激活受体α（PPARα）和成纤维细胞生长因子21（FGF21）蛋白表达水平上调，而雷帕霉素靶蛋白复合物1（mTORC1）蛋白表达水平显著下调。这些结果表明，HIIT通过改变小鼠肝脏中mTORC1、PPARα和FGF21的表达诱导肝脏酮体生成。
