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

Q3 Medicine 生理学报 Pub Date : 2024-04-25
Jun Liu, Shu-Jie Lou
{"title":"[High-intensity interval training (HIIT) induces hepatic ketone body production possibly through altering expression of mTORC1, PPARα and FGF21 in mice].","authors":"Jun Liu, Shu-Jie Lou","doi":"","DOIUrl":null,"url":null,"abstract":"<p><p>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.</p>","PeriodicalId":7134,"journal":{"name":"生理学报","volume":"76 2","pages":"224-232"},"PeriodicalIF":0.0000,"publicationDate":"2024-04-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"生理学报","FirstCategoryId":"1087","ListUrlMain":"","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"Medicine","Score":null,"Total":0}
引用次数: 0

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.

分享 分享
微信好友 朋友圈 QQ好友 复制链接
本刊更多论文
[高强度间歇训练(HIIT)可能通过改变小鼠体内 mTORC1、PPARα 和 FGF21 的表达诱导肝酮体的产生】。]
本研究旨在调查小鼠在接受 6 周高强度间歇训练(HIIT)干预后肝脏中酮体的产生情况,并探讨其可能的机制。雄性 C57BL/6J 小鼠(7 周大)被随机分为对照组和 HIIT 组。对照组不进行运动,而HIIT组则进行为期6周的HIIT(10°斜坡跑步机运动)。记录体重和身体成分的变化,并在每次 HIIT 运动前、运动后和运动后 1 小时测量血液中的酮体水平。在 6 周的 HIIT 运动后,使用试剂盒检测肝脏和血清中游离脂肪酸的水平,并通过 Western 印迹和 qPCR 检测小鼠肝脏中酮体产生的调节因子和关键酶的表达水平。结果表明,HIIT 组在单次 HIIT 后立即和 HIIT 后 1 h 的血酮体水平较 HIIT 前明显升高。对照组小鼠的体重在 6 周内逐渐增加,而 HIIT 组小鼠的体重没有明显增加。经过 6 周的 HIIT 后,与对照组相比,HIIT 组的体脂比下降,瘦体重比增加,肝脏和血清中的游离脂肪酸水平升高。与对照组相比,HIIT 组肝脏肉碱棕榈酰基转移酶Ⅰ(CPT-Ⅰ)、过氧化物酶体增殖激活受体α(PPARα)和成纤维细胞生长因子 21(FGF21)蛋白表达水平上调,而哺乳动物雷帕霉素靶复合物 1(mTORC1)蛋白表达水平显著下调。这些结果表明,HIIT 通过改变小鼠体内 mTORC1、PPARα 和 FGF21 的表达诱导肝酮体的产生。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
求助全文
约1分钟内获得全文 去求助
来源期刊
生理学报
生理学报 Medicine-Medicine (all)
CiteScore
1.20
自引率
0.00%
发文量
4820
期刊介绍: Acta Physiologica Sinica (APS) is sponsored by the Chinese Association for Physiological Sciences and Shanghai Institutes of Biological Sciences, Chinese Academy of Sciences (CAS), and is published bimonthly by the Science Press, China. APS publishes original research articles in the field of physiology as well as research contributions from other biomedical disciplines and proceedings of conferences and symposia of physiological sciences. Besides “Original Research Articles”, the journal also provides columns as “Brief Review”, “Rapid Communication”, “Experimental Technique”, and “Letter to the Editor”. Articles are published in either Chinese or English according to authors’ submission.
期刊最新文献
[Exogenous EPO protects HT22 cells from intermittent hypoxia-induced injury by activating JAK2-STAT5 signaling pathway]. [m6A RNA methylation is a potential biological target for neuropathic pain]. [Research progress in the regulation of functional homeostasis of adipose tissue by exosomal miRNA]. [Research progress of human induced pluripotent stem cells in the establishment and application of dilated cardiomyopathy disease model]. [Research progress of the effects of high-intensity interval training on excess post-exercise oxygen consumption in human].
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
现在去查看 取消
×
提示
确定
0
微信
客服QQ
Book学术公众号 扫码关注我们
反馈
×
意见反馈
请填写您的意见或建议
请填写您的手机或邮箱
已复制链接
已复制链接
快去分享给好友吧!
我知道了
×
扫码分享
扫码分享
Book学术官方微信
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术
文献互助 智能选刊 最新文献 互助须知 联系我们:info@booksci.cn
Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。
Copyright © 2023 Book学术 All rights reserved.
ghs 京公网安备 11010802042870号 京ICP备2023020795号-1