由于ACOT1缺乏,通过增加能源消耗,减轻高脂肪饮食引起的脂肪量增加
Timothy D Heden1, Mallory P Franklin2, Christina Dailey2
1Pennington Biomedical Research Center, Baton Rouge, Louisiana, USA.
JCI insight
|August 10, 2023
概括
向乙-CoA thioesterase 1 (ACOT1) 可能可以预防肥胖. ACOT1淘汰赛小鼠通过增加能量消耗来保护高脂肪饮食引起的肥胖.
科学领域:
- 代谢研究的研究.
- 肥胖研究的研究.
- 线粒体功能 线粒体功能
背景情况:
- 乙-CoA thioesterase 1 (ACOT1) 水解长链乙-CoAs,并且在肥胖症中被上调.
- 在肥胖症中准ACOT1的治疗潜力仍然未被探索.
研究的目的:
- 为了研究针对高脂肪饮食引起的肥胖症中的ACOT1的代谢益处.
- 阐明ACOT1在能源支出和重量调节中的作用背后的机制.
主要方法:
- 产生和分析ACOT1淘汰赛 (ACOT1KO) 食高脂肪饮食 (HFD) 的小鼠.
- 评估能源消耗,体力活动和食物摄入量.
- 测量线粒体解蛋白-2 (UCP2) 和氧化应激标志物.
- 肝细胞研究涉及ACOT1淘汰 (KD) 和UCP2淘汰.
主要成果:
- ACOT1KO小鼠表现出对HFD诱导的肥胖症的部分保护.
- 保护与增加的能量消耗有关,独立于身体活动或食物摄入.
- 在雄性小鼠中,ACOT1缺乏增加了UCP2并减少了氧化应激.
- 在肝细胞中UCP2敲击取消了ACOT1 KD诱导的氧气消耗增加.
结论:
- 准ACOT1可能是一个可行的策略,在卡路里过剩期间预防肥胖.
- 增加的能量消耗,可能由UCP2诱导的线粒体解介导,是关键机制.
- ACOT1在调节能量平衡和减轻饮食引起的体重增加方面发挥着重要作用.
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