在冷水中游泳会通过减少Myostatin通路来加快色过程
Niloofar Rahmani1, Pezhman Motamedi2, Sadegh Amani-Shalamzari1
1Department of Exercise Physiology, Faculty of Physical Education and Sports Science, Kharazmi University, Tehran, Iran.
Molecular biology reports
|August 2, 2024
概括
在老鼠中,在冷水中游泳六周增强了脂肪组织的色. 这与运动相结合,显示了对发热基因表达和肌静素抑制的附加效应,促进了能量消耗.
科学领域:
- 生理学 生理学 生理学
- 代谢过程中的代谢.
- 内分泌学 在内分泌学.
背景情况:
- 棕色脂肪组织 (BAT) 通过不发的热生成增加能量消耗.
- 众所周知,暴露于寒冷和运动促进了BAT和白色脂肪组织 (WAT) 色.
- 研究结合寒冷和运动刺激对脂肪组织色的附加效应.
研究的目的:
- 为了确定在寒冷暴露期间游泳运动对Wistar大鼠脂肪组织色标记物的添加效应.
- 分析与热生成和色相关的基因和蛋白质表达.
- 评估对体重,WAT和BAT特征的影响.
主要方法:
- 维斯塔鼠被分为控制 (25°C),中性游泳 (30°C) 和冷水游泳 (15°C) 水群.
- 六周间隔游泳 (每周3天),体重负荷为3-6%.
- 对色标志物基因表达和蛋白质水平进行骨间的BAT和 inguinal WAT分析.
主要成果:
- 在冷水中游泳 (SC) 降低了体重增加,WAT和BAT体积,同时增加了BAT数.
- 在脂肪组织中,SC显著增加了干扰素调节因子-4 (IRF4),PGC-1α和UCP1的表达.
- 在SC和SN组中,在BAT,WAT和血清中,myostatin蛋白质表达减少.
结论:
- 在Wistar大鼠中,在冷水中游泳六周会对脂肪组织色标志物产生添加效应.
- 寒冷诱导的游泳促进了发热基因表达 (PGC-1α,UCP1) 并降低了肌肉平衡素.
- 肌静素抑制可能调节参与脂肪组织色的PGC-1α-UCP1通路.
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