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低垂体FTO通过增加CX3CL1表达在小鼠中促进高脂肪饮食诱导的瘦素抵抗

Shujing Liu¹, Shiyu Song¹, Shuan Wang¹

¹Key Laboratory of Sports Technique, Tactics and Physical Function of General Administration of Sport of China, Scientific Research Center, Guangzhou Sport University, Guangzhou 510500, P.R. China.

The Journal of nutritional biochemistry

|October 31, 2023

概括

高脂肪饮食导致肥胖,因为它会在下丘脑中诱导勒素抵抗. FTO基因通过控制CX3CL1的m6A修饰来调节这个过程,影响肥胖.

科学领域:

代谢和内分泌学
分子生物学分子生物学
肥胖问题研究研究

背景情况:

长期的高脂肪饮食 (HFD) 消费会破坏能量平衡,导致肥胖.
脂肪质量和与肥胖相关的 (FTO) 基因与HFD诱导的肥胖有关.
由HFD驱动的下丘脑瘦素耐药性,对肥胖症的发展有显著的贡献.

研究的目的:

为了研究FTO基因与下丘脑勒素耐药性之间的关联.
阐明FTO影响瘦素抵抗和肥胖的分子机制.
在HFD引起的肥胖的背景下,确定FTO的下游目标.

主要方法:

雄性小鼠在22周内被食HFD或标准饮食 (SD).
采用m6A测序和西区测量来识别基因并评估蛋白质水平.
用CRISPR/Cas9基因淘汰来研究FTO在瘦素耐药性和肥胖症中的功能作用.

主要成果:

化学因子 (C-X3-C动机) 配体1 (CX3CL1) 被确定为FTO介导的m6A修饰的直接下游目标.
在下丘脑中FTO,CX3CL1和细胞因子信号传递3 (SOCS3) 抑制剂的升调会损害莱普信号传递,导致莱普抗性和肥胖.
在海马体神经元中的FTO缺陷部分改善了叶丁耐药性,并在HFD条件下降低了CX3CL1/SOCS3上调.

结论:

FTO在介导下丘脑素耐药性方面发挥着至关重要的作用.
通过调节像CX3CL1.1这样的目标基因的m6A修饰,FTO会影响肥胖.
这项研究提供了关于FTO在下丘脑白抗性和肥胖发展中的作用的新见解.

关键词:

在CX3CL1中.在 FTO FTO FTO.下丘脑的下丘脑是什么意思有高脂肪的饮食.勒普丁耐药性勒普丁耐药性是一种

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