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在急性寒冷暴露后,多层调节食后甘油三代谢以应对急性寒冷暴露
Yiliang Zhang1, Shengyang Zhou1, Runming Zhao1
1State Key Laboratory of Metabolism and Regulation in Complex Organisms, Hubei Key Laboratory of Cell Homeostasis, College of Life Sciences, TaiKang Center for Life and Medical Sciences, Wuhan University, Wuhan, China.
Journal of lipid research
|February 1, 2025
概括
急性感冒暴露会降低血中甘油三水平,因为它增强了清除,而不是产量. 这涉及棕色脂肪的吸收增加和白色脂肪的吸收减少,由ANGPTL蛋白调节.
科学领域:
- 代谢调节 代谢调节 代谢调节
- 脂质新陈代谢 脂质新陈代谢
- 热调节 热调节 热调节
背景情况:
- 富含三糖蛋白的脂蛋白是主要的脂质载体.
- 高甘油和残留颗粒是心血管疾病的风险.
- 急性感冒暴露可能治疗高甘油三血症,但机制尚不清楚.
研究的目的:
- 研究急性寒冷暴露如何调节三糖代谢.
- 阐明脂肪组织和特定蛋白质在这个过程中的作用.
主要方法:
- 研究了暴露于寒冷的小鼠来分析非常低密度脂蛋白的产生和甘油三清除.
- 评估了棕色脂肪组织 (BAT) 和白色脂肪组织 (WAT) 中的脂蛋白脂酶 (LPL) 活性和甘油三的吸收.
- 使用淘汰赛小鼠和分子分析检查了ANGPTL3,ANGPTL4和ANGPTL8的作用.
主要成果:
- 寒冷暴露增加了食后非常低密度脂蛋白的产生和甘油三清除,清除占主导地位.
- 最佳技术显示LPL活动和TG吸收增加,而WAT显示LPL活动和TG吸收抑制.
- 机制涉及通过胰岛素-ANGPTL8-ANGPTL3轴和通过ANGPTL4.4抑制WAT通过BAT的LPL上调.
- ANGPTL8 缺乏消除了寒冷诱导的 TG 减少,增加了寒冷暴露后的 TG 水平.
结论:
- 急性寒冷暴露调节了食后甘油三代谢的复杂调节.
- 在BAT和WAT中LPL活动的平衡,由ANGPTL蛋白调节,至关重要.
- ANGPTL3,ANGPTL4和ANGPTL8是感冒诱导的代谢反应的关键调解者.
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