Author:
Qin Yongli,Jia Lina,Liu Huijiao,Ma Wenqiang,Ren Xinmin,Li Haifeng,Liu Yuanwu,Li Haiwen,Ma Shuoqian,Liu Mei,Li Pingping,Yan Jinghua,Zhang Jiyan,Guo Yangdong,You Hua,Guo Yan,Rahman Nafis A.,Wołczyński Sławomir,Kretowski Adam,Li Dangsheng,Li Xiru,Ren Fazheng,Li Xiangdong
Abstract
AbstractIn obesity, macrophages drive a low-grade systemic inflammation (LSI) and insulin resistance (IR). The ribosome biosynthesis protein NOC4 (NOC4) mediates 40 S ribosomal subunits synthesis in yeast. Hereby, we reported an unexpected location and function of NOC4L, which was preferentially expressed in human and mouse macrophages. NOC4L was decreased in both obese human and mice. The macrophage-specific deletion of Noc4l in mice displayed IR and LSI. Conversely, Noc4l overexpression by lentivirus treatment and transgenic mouse model improved glucose metabolism in mice. Importantly, we found that Noc4l can interact with TLR4 to inhibit its endocytosis and block the TRIF pathway, thereafter ameliorated LSI and IR in mice.
Funder
CAU | State Key Laboratory of Agrobiotechnology, China Agricultural University
Publisher
Springer Science and Business Media LLC
Subject
General Physics and Astronomy,General Biochemistry, Genetics and Molecular Biology,General Chemistry
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