脂肪酸通过白色脂肪细胞中的ATP/ADP载体促进脱呼吸
Maryam Ahmadian1, A Melisa Aksu2, Preetveer Dhillon2
1Division of Metabolism and Endocrinology, Department of Medicine, University of California San Diego, La Jolla, CA, USA.
自由脂肪酸通过驱动白色脂肪细胞的脱呼吸来增加能量消耗,这是治疗肥胖症的关键发现. 这一过程增强了热生成,即使在肥胖的情况下,也提供了新的治疗点.
科学领域:
- 代谢过程中的代谢.
- 细胞呼吸 细胞呼吸
- 脂肪细胞生物学 脂肪细胞生物学
背景情况:
- 脂肪细胞以甘油三的形式储存能量,通过脂解释放脂肪酸.
- 脂肪细胞内脂肪酸的重新化消耗ATP,并矛盾地抑制呼吸.
- 之前已经证明,STAT3 (信号转换器和转录3激活器) 通过抑制再化来促进呼吸.
研究的目的:
- 为了研究自由脂肪酸在驱动脂肪细胞脱呼吸中的作用.
- 为了确定白色脂肪细胞脱呼吸对热生成的贡献,特别是在肥胖症中.
- 探索与脂肪细胞能量消耗相关的肥胖症治疗的潜在治疗目标.
主要方法:
- 在各种条件下对脂肪细胞中脱呼吸的分析.
- 调查自由脂肪酸,脂肪乙烯-CoAs和β-氧化在呼吸中的作用.
- 在小鼠的棕色和白色脂肪细胞中评估发热通路,包括肥胖模型.
主要成果:
- 自由脂肪酸直接刺激不结合的呼吸,独立于脂肪乙-CoAs或β-氧化.
- 白色脂肪细胞中不结合的呼吸对肥胖的,适应热中性的小鼠的热生成和耐寒性有显著的贡献.
- 这种贡献独立于棕色脂肪组织和肌肉活动.
结论:
- 白色脂肪细胞中不结合的呼吸是全身能量消耗的重要途径.
- 针对白色脂肪细胞的脱呼吸可能为肥胖症治疗提供一种新的策略.
- 脂肪酸是通过脱呼吸来调节脂肪细胞能量消耗的关键调节者.
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