脂肪细胞中的Fas (CD95) 表达有助于饮食诱导的肥胖
Stephan Wueest1,2, Chiara Scaffidi1,2, Pim P van Krieken1,2
1Division of Pediatric Endocrinology and Diabetology, University Children's Hospital, University of Zurich, Zurich, Switzerland.
Obesity (Silver Spring, Md.)
|July 18, 2024
概括
禁食诱导的脂肪细胞Fas激活通过抑制白色脂肪组织色而促进肥胖. 阻断脂肪细胞中的Fas可能为肥胖和相关代谢障碍提供一种新的治疗策略.
科学领域:
- 脂肪组织生物学 脂肪组织生物学
- 代谢性疾病研究研究.
- 肥胖治疗方法 肥胖治疗方法
背景情况:
- 白色脂肪组织 (WAT) 色增加能量消耗,成为潜在的肥胖治疗标.
- 酶 (CD95) 激活可以抑制脱蛋白1 (UCP1) 表达,这是棕色脂肪组织中热生成的关键媒介.
- Fas在调节WAT棕色化中的作用及其对肥胖的贡献仍然不清楚.
研究的目的:
- 调查Fas在脂肪细胞中的表达抑制WAT色并导致肥胖发展的假设.
- 探索Fas信号作为肥胖的潜在治疗点.
主要方法:
- 产生的脂肪细胞特异性Fas淘汰赛 (FasΔadipo) 小鼠和子期对照 (FasF/F).
- 在20周的高脂肪饮食 (HFD) 中,通过间接热量计和WAT棕色化来评估能量消耗.
- 分析了用Fas连接体治疗的培养脂肪细胞中的UCP1表达和与UCP1和身体脂肪百分比相关的人类WAT FAS表达.
主要成果:
- 与对照组相比,在HFD上的FasΔadipo小鼠表现出体重增加和脂肪减少.
- 在FasDadipo小鼠中,全身能量消耗和WAT色显著增加.
- 联剂治疗降低了培养脂肪细胞中的UCP1水平;人类研究显示了FAS和UCP1之间的负相关性,以及与脂肪的正相关性.
结论:
- 脂肪细胞中的Fas激活促进动物的饮食诱导肥胖.
- 向脂肪细胞中的Fas可能代表了一种新的治疗方法,用于管理肥胖和相关的代谢条件.
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