血管性血友病因子缺乏症可改善高脂饮食喂养小鼠的肝脂肪变性、胰岛素抵抗和炎症。
Von Willebrand Factor Deficiency Improves Hepatic Steatosis, Insulin Resistance, and Inflammation in Mice Fed High-Fat Diet.
机构信息
Department of Endocrinology, Huadong Hospital Affiliated to Fudan University, Shanghai, PR China.
The Shanghai Key Laboratory of Clinical Geriatric Medicine, Shanghai, PR China.
出版信息
Obesity (Silver Spring). 2020 Apr;28(4):756-764. doi: 10.1002/oby.22744. Epub 2020 Mar 6.
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.
目的
本研究旨在探讨血管性血友病因子（VWF）对高脂肪饮食（HFD）诱导的小鼠肝脂肪变性、胰岛素抵抗和炎症的影响。
方法
检测肥胖小鼠中 VWF 的表达。将野生型和 VWF 敲除小鼠分别喂食正常饲料或 HFD，然后进行生物医学、组织学和代谢分析，以确定病理改变。在这些喂食 HFD 的小鼠中测定炎性细胞因子水平和肝巨噬细胞数量。
结果
肥胖小鼠中 VWF 的表达显著增加。VWF 小鼠肥胖程度降低，对 HFD 反应的肝脂肪变性、脂质代谢平衡和胰岛素抵抗得到改善。此外，VWF 缺乏可减轻 HFD 诱导的全身和肝脏炎症。此外，VWF 缺乏可纠正肝巨噬细胞的异常积累。
结论
这些数据表明 VWF 缺乏可改善肝脂肪变性、胰岛素抵抗和炎症。此外，保护作用是通过调节肝巨噬细胞介导的。
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