酸化减弱了CPT-I支持的生物能量,作为限制脂质氧化的潜在机制
Sara M Frangos1, Geneviève J DesOrmeaux1, Graham P Holloway1
1Department of Human Health and Nutritional Sciences, University of Guelph, Guelph, Ontario, Canada.
The Journal of biological chemistry
|July 23, 2023
概括
运动诱导的肌肉酸化通过抑制关键酶卡尼丁棕转移酶-I (CPT-I) 来损害脂肪酸氧化. 碳水化合物代谢受到的影响较小,这解释了强度运动期间的燃料转移.
科学领域:
- 肌肉生理学 肌肉生理学
- 线粒体的生物能量学
- 代谢调节 代谢调节 代谢调节
背景情况:
- 肌肉收缩涉及复杂的燃料相互作用,碳水化合物使用量增加,脂肪酸氧化在更高的运动强度下降.
- 驱动这种燃料转移的确切机制尚不清楚.
研究的目的:
- 为了调查运动诱导的肌肉酸性损伤 (降低的pH值) 是否会影响卡尼丁棕转移酶-I (CPT-I) 的活性,这是脂肪酸氧化过程中限制速度的步骤.
- 通过使用不同的燃料基板来评估化对线粒体呼吸的影响.
主要方法:
- 评估了pH值7.2与6.8对隔离的小鼠骨肌肉线粒体和透纤维的影响.
- 测量单基质和混合基质的呼吸反应,氧化酸化效率和酶动力学.
- 在休息和强度运动后检查的效果.
主要成果:
- 酸性酶通过减少用L-卡尼丁和棕醇-CoA的呼吸和增加CPT-I. malonyl-CoA抑制来降低脂质生物能效.
- 这些影响在强度炼后仍然存在.
- 虽然酸化也损害了静止碳水化合物氧化,但在低pH下增加的基质可用性 (pyruvate,ADP) 补偿了碳水化合物相关的氧化酸化.
- 通过CPT-I进行的脂质代谢显示,比碳水化合物代谢更容易发生酸化.
结论:
- 运动诱导的酸化会通过抑制CPT-I.I.来损害线粒体脂肪酸氧化.
- 与碳水化合物代谢不同的是,这种脂质代谢的损害可能有助于在高强度运动期间转向碳水化合物利用.
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