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MOL CELL:饥饿为何也能引起脂肪肝?

2020-06-10 MedSci原创 MedSci原创

已有的研究显示,自噬能够被长期禁食激活,但不能克服随之而来的肝脏脂质超载,导致脂肪肝。

已有的研究显示,自噬能够被长期禁食激活,但不能克服随之而来的肝脏脂质超载,导致脂肪肝。

最近,研究人员发现了一个限制自噬降解脂质的过氧体-溶酶体代谢环节。酰基辅酶A氧化酶1(Acox1)是催化过氧体β-氧化的第一步的酶,其在肝脏中富集,并随着空腹或高脂饮食(HFD)进一步增加。

肝脏特异性Acox1基因敲除(Acox1-LKO)可保护小鼠免受饥饿或HFD引起的肝脏脂肪变性,原因是诱导脂滴的自噬降解。肝脏Acox1缺失明显降低了细胞总乙酰辅酶A水平,导致Raptor蛋白乙酰化减少,mTOR的溶酶体定位减少,导致自噬的中枢调节因子mTORC1的激活受损。

二氯乙酸处理可提高乙酰辅酶A水平,恢复mTORC1激活,抑制自噬,并增加Acox1-LKO小鼠的肝脏甘油三酯。

这些结果确定了过氧化物酶体衍生的乙酰辅酶A是控制肝脏脂质稳态的自噬的关键代谢调节剂。

 

原始出处:

Anyuan He et al. Acetyl-CoA Derived from Hepatic Peroxisomal β-Oxidation Inhibits Autophagy and Promotes Steatosis via mTORC1 Activation. Molecular Cell (2020). DOI:https://doi.org/10.1016/j.molcel.2020.05.007

 

 

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