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在小鼠中,Wnt10b knockdown 在棕色脂肪组织中促进了 UCP1 的表达

Yanxin Jia¹, Yan Liu¹, Shuang Liu²

¹State Key Laboratory of Crop Biology, College of Life Sciences, Shandong Agricultural University, Tai'an, China.

Genes to cells : devoted to molecular & cellular mechanisms

|September 11, 2023

概括

在小鼠中Wnt10b Knockdown降低了棕色脂肪的大小,但增加了热源基因UCP1的表达. 这改善了寒冷耐受性和减轻了肥胖症,表明Wnt10b抑制是治疗肥胖症的治疗策略.

科学领域:

代谢和内分泌学
脂肪组织生物学脂肪组织生物学
分子遗传学分子遗传学

背景情况:

已知Wnt10b对脂肪组织的过度表达效应.
Wnt10b在棕色脂肪组织 (BAT) 功能中的作用在很大程度上仍未被探索.

研究的目的:

为了研究Wnt10b淘汰对棕色脂肪组织 (BAT) 发育和功能的影响.
在各种饮食和环境条件下,评估Wnt10b缺乏对发热和肥胖的影响.

主要方法:

使用CRISPR/Cas9技术制造了Wnt10b-knockdown (Wnt10b+/-) 的小鼠.
在Wnt10b+/-和对照 (Wnt10b+/+) 食,高脂肪饮食 (HFD) 和寒冷暴露的小鼠中,对骨间的BAT (iBAT) 的比较分析.
关于棕色脂肪细胞功能的体外研究.

主要成果:

在食饮食中,Wnt10b的淘汰降低了iBAT质量和棕色脂肪细胞大小,但增强了发热基因表达 (例如,UCP1).
Wnt10b+/-小鼠在寒冷条件下表现出改善的体温调节,同时增加了UCP1蛋白.
尽管HFD,但Wnt10b+/-小鼠保持了更高的UCP1表达,并显示了减轻的肥胖现型.
在体外实验证实了Wnt10b的Knockdown刺激UCP1的表达和抑制基分化.

结论:

Wnt10b knockdown 增强了 UCP1 的表达,并抑制了棕色脂肪细胞中的脂肪原分化.
这表明Wnt10b抑制是治疗肥胖和相关代谢障碍的潜在治疗方法.

关键词:

在UCP1中,UCP1是UCP1.在 Wnt10bb 中使用.棕色脂肪组织 (BAT)不同化的差异化差异化.热生成是一种热生成.

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