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核因子介质素3和与代谢功能障碍相关的脂肪肝疾病的发展

Yung-Ni Lin¹, Jia-Rou Hsu¹, Chih-Lin Wang¹

¹Department and Institute of Physiology, College of Medicine, National Yang Ming Chiao Tung University, Taipei, Taiwan.

Communications biology

|July 24, 2024

概括

在小鼠中删除Nfil3基因可以通过改善肠道屏障功能和改变胆酸概况来降低代谢功能障碍相关的脂肪性肝病 (MASLD) 的严重程度. 这表明Nfil3抑制是对MASLD的潜在治疗方法.

科学领域:

代谢性疾病研究研究.
肝病学肝病学是一种肝病学.
免疫学免疫学免疫学

背景情况:

与代谢功能障碍相关的脂肪性肝病 (MASLD) 是一个日益严重的健康问题.
在饮食引起的肝病和肠道微生物群改变中Nfil3的作用尚未完全理解.
对代谢挑战的性别特异性反应需要进一步研究.

研究的目的:

调查Nfil3缺乏对高脂肪饮食 (HFD) 诱导的性别特异性影响.
评估Nfil3对肠道微生物群 (GM) 组成和胆酸 (BA) 概况的影响.
探索MASLD中Nfil3抑制的治疗潜力.

主要方法:

使用高脂肪饮食 (HFD) 诱导野生型和Nfil3缺乏 (NKO) 老鼠的MASLD.
通过流细胞计对肝脏免疫反应的评估.
对肠道微生物群多样性和胆酸概况的分析.
评估与炎症和肠道屏障功能相关的基因和蛋白质表达.

主要成果:

与对照组相比,NKO小鼠的体重,血清甘油三,肝损伤,炎症和脂肪积累减少.
删除Nfil3减少了巨细胞在纤维性肝脏组织中的透,并抑制了前炎性标志物.
基因转基因α多样性在不同性别的NKO小鼠中增加,BA概况发生显著变化.
缺少Nfil3调节了Nfil3-FXR-FGF15轴,影响了胆酸循环.

结论:

在HFD诱导的MASLD的发病过程中,Nfil3起着重要作用.
缺乏Nfil3可以通过调节免疫反应,肠道微生物群和胆酸代谢来保护MASLD.
准Nfil3是MASLD治疗的一个有前途的治疗策略.

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