Von Willebrand Factor Deficiency Improves Hepatic Steatosis, Insulin Resistance, and Inflammation in Mice Fed High-Fat Diet
文献类型： 外文期刊
作者： Yang, Juan 1 ; Lu, Yan 1 ; Lou, Xudan 1 ; Wang, Jian 3 ; Yu, Huilin 4 ; Bao, Zhijun 2 ; Wang, Haidong 1 ;
作者机构： 1.Fudan Univ, Huadong Hosp, Dept Endocrinol, Shanghai, Peoples R China
2.Shanghai Key Lab Clin Geriatr Med, Shanghai, Peoples R China
3.Shanghai Acad Agr Sci, Inst Anim Husb & Vet Sci, Shanghai, Peoples R China
4.Fudan Univ, Jingan Dist Ctr Hosp Shanghai, Dept Translat Neurosci, State Key Lab Med Neurobiol, Shanghai, Peoples R China
5.Fudan Univ, MOE Frontiers Ctr Brain Sci, Inst Brain Sci, Shanghai, Peoples R China
6.Fudan Univ, Huadong Hosp, Dept Gastroenterol, Shanghai, Peoples R China
7.Fudan Univ, Res Ctr Aging & Med, Shanghai, Peoples R China
8.Fudan Univ, Huadong Hosp, Dept Geriatr, Shanghai, Peoples R China
期刊名称：OBESITY （ 影响因子：5.002； 五年影响因子：5.251 ）
ISSN： 1930-7381
年卷期： 2020 年 28 卷 4 期
页码：
收录情况： SCI
摘要： Objective The aim of this study was to investigate the effect of Von Willebrand factor (VWF) on high-fat diet (HFD)-induced hepatic steatosis, insulin resistance, and inflammation in mice. Methods The expression of VWF was detected in obese mice. Wild-type and VWF knockout mice were fed a normal chow diet or an HFD, and then biomedical, histological, and metabolic analyses were conducted to identify pathologic alterations. Inflammatory cytokine levels and the number of hepatic macrophages were determined in these mice fed an HFD. Results VWF expression was significantly increased in obese mice. VWF-/- mice were less obese and had improved hepatic steatosis, balance of lipid metabolism, and insulin resistance in response to HFD. Furthermore, VWF deficiency attenuated HFD-induced systemic and hepatic inflammation. In addition, VWF deficiency rescued the abnormal accumulation of hepatic macrophages. Conclusions These data demonstrated VWF deficiency improves hepatic steatosis, insulin resistance, and inflammation. Furthermore, the protective effects are mediated via regulation of hepatic macrophages.
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