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Inhibition of PU.1 ameliorates metabolic dysfunction and non-alcoholic steatohepatitis by Qiongming Liu; Junjie Yu; Liheng Wang; Yuliang Tang; Quan Zhou; Shuhui Ji; Yi Wang; Luis Santos; Rebecca A. Haeusler; Jianwen Que; Prashant Rajbhandari; Xiaoguang Lei; Luca Valenti; Utpal B. Pajvani; Jun Qin; Li Qiang is a Medicine article available to read on EtoBox.

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## Background & aims: Obesity is a well-established risk factor for type 2 diabetes (t2d) and non-alcoholic steatohepatitis (nash), but the underlying mechanisms remain incompletely understood. herein, we aimed to identify novel pathogenic factors (and possible therapeutic targets) underlying metabolic dysfunction in the liver. ## Methods: We applied a tandem quantitative proteomics strategy to enrich and identify transcription factors (tfs) induced in the obese liver. we used flow cytometry of liver cells to analyze the source of the induced tfs. we employed conditional knockout mice, shrna, and small-molecule inhibitors to test the metabolic consequences of the induction of identified tfs. finally, we validated mouse data in patient liver biopsies. ## Results: We identified pu.1/spi1, the master hematopoietic regulator, as one of the most upregulated tfs in livers from diet-induced obese (dio) and genetically obese (db/db) mice. targeting pu.1 in the whole liver, but not hepatocytes alone, significantly improved glucose homeostasis and suppressed liver inflammation. consistently, treatment with the pu.1 inhibitor db1976 markedly reduced inflammation and improved glucose homeostas

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Author

Qiongming Liu; Junjie Yu; Liheng Wang; Yuliang Tang; Quan Zhou; Shuhui Ji; Yi Wang; Luis Santos; Rebecca A. Haeusler; Jianwen Que; Prashant Rajbhandari; Xiaoguang Lei; Luca Valenti; Utpal B. Pajvani; Jun Qin; Li Qiang

Publisher

Elsevier Science; Elsevier ; Elsevier BV; Wiley (ISSN 0168-8278)

Published

2020

Language

EN

Field

Medicine (Health Sciences)