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在实验室中,LEP通过AMPK信号通路抑制肌内脂肪生成

Shengchen Yu¹, Hengwei Yu¹, Jianfang Wang¹

¹College of Animal Science and Technology, Northwest A&F University, Yangling, China.

FASEB journal : official publication of the Federation of American Societies for Experimental Biology

|July 24, 2024

概括

素 (LEP) 通过通过AMPK信号通路调节脂肪细胞的增殖和分化来抑制牛肉肌内脂肪的产生. 这项研究澄清了LEP.

科学领域:

动物科学动物科学
分子生物学分子生物学
生物化学生物化学

背景情况:

莱普 (LEP) 影响肌肉中的脂肪酸代谢.
牛LEP基因的突变与肌肉内脂肪 (IMF) 含量相关.
对于LEP对脂肪细胞脂质合成的细胞水平影响尚不清楚.

研究的目的:

调查LEP对牛肌内前脂细胞增殖和分化的影响.
阐明LEP在细胞水平的脂质合成中的调节机制.
确定LEP在AMPK信号通路中的作用.

主要方法:

研究了牛初级肌肉前脂肪细胞.
分析了LEP和瘦素受体基因 (LEPR) 的mRNA表达.
使用LEP过度表达和干扰技术.
用AMPK抑制剂进行了救援实验.

主要成果:

LEP和LEPR在IMF组织中高度表达,并在前脂肪细胞发育过程中具有积极的相关性.
LEP过度表达抑制了前脂细胞的增殖和分化;LEP干扰显示了相反的效果.
通过上调CAMKK2蛋白表达的调节,LEP促进了AMPKα酸化.
过度表达LEP减弱了AMPK抑制剂对前脂质细胞数量,甘油三含量和脂肪基因/蛋白质表达的影响.

结论:

通过CAMKK2.2,LEP通过AMPK信号通路对肌肉内脂肪生成进行调节.
LEP降低了与增殖和脂肪生成相关的基因和蛋白质的下调,减少了肌肉内脂肪沉积.
这些发现为LEP在牛脂质代谢中的作用提供了细胞层面的见解.

关键词:

对于LEP来说,这是一个很好的选择.AMPK信号通道的信号通道.脂质生成 (adipogenesis) 是一种肌肉内预皮细胞

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