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宿主酶通过非活化肠道脂多糖化合物来减少与代谢功能障碍相关的脂肪性肝病 (MASLD)
Zhiyan Wang1, Nore Ojogun2, Yiling Liu1
1Department of Immunology, School of Basic Medical Sciences, Department of Trauma-Emergency & Critical Care Medicine, Shanghai Fifth People's Hospital, Fudan University, Shanghai, China.
缺乏乙氧酸酶 (AOAH) 的小鼠积累了更多的肝脂肪,表明AOAH缺乏会恶化与代谢功能障碍相关的脂肪性肝病 (MASLD). 增加AOAH可以预防或治疗这种情况.
科学领域:
- 肝病学 肝病学是一种肝病学.
- 代谢疾病 代谢疾病
- 脂质代谢 脂质代谢是什么
背景情况:
- 与代谢功能障碍相关的脂肪性肝病 (MASLD) 发病率在全球范围内正在上升.
- 来自肠道的脂聚糖 (LPS) 导致肝脏病理.
- 乙酸酸酶 (AOAH) 禁用了LPS和氧化脂.
研究的目的:
- 调查AOAH在肝脂积累中的作用.
- 为了确定AOAH缺乏是否会加剧MASLD.
- 探索AOAH作为MASLD的潜在治疗点.
主要方法:
- 在28周的时间里,小鼠吃了正常的或高脂肪饮食.
- 测量了肝脏脂质含量.
- 与脂质代谢相关的基因表达在野生类型和Aoah缺陷小鼠中被分析.
主要成果:
- 与对照组相比,Aoah缺乏的小鼠累积的肝脂显著更多.
- 在年轻的Aoah缺乏小鼠中,增加的固醇调节元素结合蛋白1及其向基因促进了脂肪酸合成.
- 肝脂肪酸吸收基因 (Cd36,Fabp3) 被上调,而脂肪酸氧化基因 (Acot2,Ppara) 在Aoah缺乏的小鼠中被下调.
结论:
- 缺少AOAH会促进肝脏脂质的积累,并加剧MASLD.
- 调节AOAH水平可能是预防或治疗MASLD的新策略.
- 针对肠道,血液或肝脏中的AOAH可能为MASLD提供治疗益处.
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