人类骨肌肉中的乙基-CoA合成酶表达在肥胖和胰岛素耐药性下降
Margarete Poppelreuther1, Anne-Marie Lundsgaard2, Pernille Mensberg3
1Molecular Cell Biology Laboratory, Internal Medicine IV, University of Heidelberg, Heidelberg, Germany.
Physiological reports
|September 19, 2023
概括
患有2型糖尿病的肥胖个体在骨肌肉中脂肪乙-CoA合成酶 (ACS) 酶活性较低,阻碍脂肪酸转化. 在这些人中,运动训练改善了ACS活动和胰岛素敏感性.
科学领域:
- 生物化学 生物化学
- 代谢健康 代谢健康
- 运动生理学 运动生理学
背景情况:
- 脂肪酸通过肌肉中的-A合成酶 (ACS) 转化为脂肪-CoA.
- 骨肌肉中的胰岛素抵抗与脂肪-CoA的积累有关,但ACS酶的作用尚未得到充分研究,特别是在肥胖和T2D方面.
- 长链乙基-CoA合成酶1 (ACSL1) 是人类骨肌肉中的主要ACS异型.
研究的目的:
- 研究人类骨肌中的ACS酶的表达和活性,从具有不同BMI和胰岛素耐药性的个体.
- 确定肥胖和2型糖尿病 (T2D) 对ACS mRNA水平和酶活性的影响.
- 评估运动训练对肥胖和T2D患者的ACS活性和胰岛素敏感性的影响.
主要方法:
- 对正常体重,肥胖和患有T2D的肥胖个体的肌肉活检进行分析.
- 使用实时PCR进行ACS mRNA表达 (ACSL1,ACSL3,ACSL4,FATP1,FATP4) 的量化.
- 测量了总的Oleoyl-CoA合成酶活性和HOMA-IR指数.
- 在患有T2D的肥胖者群体中,对16周的运动训练反应的评估.
主要成果:
- 与对照人群相比,肥胖和T2D患者的骨肌肉中总ACS mRNA和ACSL1 mRNA水平明显较低.
- ACSL1被确定为人类骨肌肉中主要表达的ACS异型.
- 肥胖和T2D患者的运动训练导致总ACS酶活性增加和HOMA-IR降低,表明胰岛素敏感性得到改善.
结论:
- 在肥胖和T2D患者中,骨肌肉对脂肪乙-CoA合成的能力降低,这表明脂肪酸转化受损.
- 在肥胖和胰岛素耐药性中脂肪乙烯-CoA的积累不太可能是由于脂肪酸乙烯化增加.
- 运动诱导的ACS活性上调是有益的,与增强的胰岛素敏感性相关.
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