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高强度间歇训练(HIIT)可能通过改变小鼠mTORC1、PPARα和FGF21表达诱导肝酮体生成

刘俊, 娄淑杰^*

上海体育大学运动健康学院，上海 200438

摘要

本文旨在研究6周高强度间歇训练(high-intensity interval training, HIIT)干预后小鼠肝脏酮体生成情况，并探讨可能的作用机制。将7周龄雄性C57BL/6J小鼠随机分为对照组和HIIT组，对照组不进行运动，而HIIT组接受为期6周HIIT (坡度为10°的跑台运动)，记录体重和体成分的变化，在一次HIIT运动前、运动后即刻、运动后1 h检测血液酮体水平。6周HIIT后，用试剂盒检测肝脏和血清中游离脂肪酸的水平，用qPCR和Western blot检测小鼠肝脏酮体生成调节因子和关键酶表达情况。结果显示，与HIIT前相比，一次HIIT后即刻、HIIT后1 h HIIT组小鼠血酮体水平显著上升。对照组小鼠的体重在6周内逐渐增加，HIIT组小鼠体重没有显著增加。6周HIIT结束之后，与对照组相比，HIIT组体脂比显著降低，而瘦体重占比显著增加，肝脏和血清游离脂肪酸水平显著升高，肝脏肉碱棕榈酰转移酶-I (carnitine palmitoyl transferase-I, CPT-I)、过氧化物酶体增殖物激活受体α (peroxisome proliferator-activated receptor α, PPARα)和成纤维细胞生长因子21 (fibroblast growth factor 21, FGF21)蛋白表达水平显著上调，哺乳动物雷帕霉素靶蛋白复合体1 (mammalian target of rapamycin complex 1, mTORC1)蛋白表达显著下调。以上结果提示，HIIT可能通过改变mTORC1、PPARα和FGF21表达来诱导小鼠肝酮体的生成。

关键词： 高强度间歇训练; 酮体; mTORC1; PPARα; FGF21

High-intensity interval training (HIIT) induces hepatic ketone body production possibly through altering expression of mTORC1, PPARα and FGF21 in mice

LIU Jun, LOU Shu-Jie^*

School of Exercise and Health, Shanghai University of Sport, Shanghai 200438, China

Abstract

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.

Key words: high-intensity interval training; ketone body; mTORC1; PPARα; FGF21

收稿日期：　　录用日期：

通讯作者：娄淑杰　　E-mail: shujielou319@163.com

DOI: 10.13294/j.aps.2024.0023

引用本文：

刘俊, 娄淑杰. 高强度间歇训练(HIIT)可能通过改变小鼠mTORC1、PPARα和FGF21表达诱导肝酮体生成[J]. 生理学报 2024; 76 (2): 224-232.

LIU Jun, LOU Shu-Jie. High-intensity interval training (HIIT) induces hepatic ketone body production possibly through altering expression of mTORC1, PPARα and FGF21 in mice. Acta Physiol Sin 2024; 76 (2): 224-232 (in Chinese with English abstract).