脂肪生成
胰岛素抵抗
脂肪变性
脱磷
内科学
下调和上调
内分泌学
磷酸酶
蛋白质亚单位
化学
蛋白磷酸酶2
胰岛素
磷酸化
生物
生物化学
脂质代谢
医学
基因
作者
Zhenyu Yao,Ying Gong,Wenbin Chen,Shanshan Shao,Yongfeng Song,Honglin Guo,Qihang Li,Sijin Liu,Ximing Wang,Zhenhai Zhang,Qian Wang,Yunyun Xu,Yingjie Wu,Qiang Wan,Xinya Zhao,Qiuhui Xuan,Dawei Wang,X. Lin,Jiawen Xu,Jun Liu
出处
期刊:Nature metabolism
[Nature Portfolio]
日期:2023-09-21
卷期号:5 (10): 1706-1725
被引量:39
标识
DOI:10.1038/s42255-023-00896-7
摘要
Under normal conditions, insulin promotes hepatic de novo lipogenesis (DNL). However, during insulin resistance (IR), when insulin signalling is blunted and accompanied by hyperinsulinaemia, the promotion of hepatic DNL continues unabated and hepatic steatosis increases. Here, we show that WD40 repeat-containing protein 6 (WDR6) promotes hepatic DNL during IR. Mechanistically, WDR6 interacts with the beta-type catalytic subunit of serine/threonine-protein phosphatase 1 (PPP1CB) to facilitate PPP1CB dephosphorylation at Thr316, which subsequently enhances fatty acid synthases transcription through DNA-dependent protein kinase and upstream stimulatory factor 1. Using molecular dynamics simulation analysis, we find a small natural compound, XLIX, that inhibits the interaction of WDR6 with PPP1CB, thus reducing DNL in IR states. Together, these results reveal WDR6 as a promising target for the treatment of hepatic steatosis.
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