Von Willebrand Factor Deficiency Improves Hepatic Steatosis, Insulin Resistance, and Inflammation in Mice Fed High-Fat Diet
Autor: | Haidong Wang, Yan Lu, Huilin Yu, Jian Wang, Juan Yang, Xudan Lou, Zhijun Bao |
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Rok vydání: | 2019 |
Předmět: |
Male
congenital hereditary and neonatal diseases and abnormalities medicine.medical_specialty Endocrinology Diabetes and Metabolism medicine.medical_treatment Medicine (miscellaneous) Mice Obese 030209 endocrinology & metabolism Inflammation Diet High-Fat 03 medical and health sciences Mice 0302 clinical medicine Endocrinology Insulin resistance Von Willebrand factor hemic and lymphatic diseases Internal medicine von Willebrand Factor medicine Animals 030212 general & internal medicine Mice Knockout Nutrition and Dietetics biology business.industry High fat diet Lipid metabolism medicine.disease Fatty Liver Mice Inbred C57BL Cytokine Knockout mouse biology.protein medicine.symptom Steatosis Insulin Resistance business circulatory and respiratory physiology |
Zdroj: | Obesity (Silver Spring, Md.)References. 28(4) |
ISSN: | 1930-739X |
Popis: | 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. |
Databáze: | OpenAIRE |
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