由DGAT驱动的无用的脂质循环具有明显的,但隐藏的热生成功能
Anand Kumar Sharma1, Radhika Khandelwal1, Jelena Zurkovic2
1Laboratory of Translational Nutrition Biology, Institute of Food, Nutrition and Health, ETH Zurich, 8603 Schwerzenbach, Switzerland.
Cell metabolism
|January 10, 2026
概括
脂肪组织无效脂质循环 (FLC) 提供了UCP1-独立的热生成. 这个由DGATs监管的过程,通过和AMPK激活来弥补其损失,保持核心体温.
科学领域:
- 生理学 生理学 生理学
- 代谢调节 代谢调节 代谢调节
- 哺乳动物的温度调节
背景情况:
- 温度调节是哺乳动物的一个关键的恒温过程,但除了UCP1-介导的热生成之外的潜在机制仍然不清楚.
- 虽然有效,但UCP1-介导的热生成并不必不可少,这意味着产生热量的替代途径.
研究的目的:
- 研究脂肪组织无效脂质循环 (FLC) 在UCP1-独立热生成中的作用.
- 确定FLC的分子调节剂,并了解补偿性热生成机制.
主要方法:
- 利用药物遗传学方法在哺乳动物模型中研究FLC.
- 研究了二甲基甘油酸转移酶 (DGATs) 在调节FLC中的参与.
- 在FLC缺陷模型中评估了补偿性热能反应,包括和AMPK激活.
主要成果:
- 证明脂肪组织的FLC对UCP1-独立的热生成有显著的贡献.
- 确定了DGAT作为FLC的关键监管机构.
- 表明DGAT驱动的FLC损失通过增加和AMPK介导的脂质代谢来补偿.
- 在FLC缺乏的小鼠中,药理上抑制发或AMPK导致能耗减少和低温.
结论:
- FLC具有显著的热能潜力,为UCP1-介导的热量生产提供了替代方案.
- 哺乳动物的温度调节表现出灵活性,通过脂肪细胞代谢变化适应维持核心体温.
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