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首页> 外文期刊>The Journal of Nutritional Biochemistry >A mouse model for nonalcoholic steatohepatitis.
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A mouse model for nonalcoholic steatohepatitis.

机译：非酒精性脂肪性肝炎的小鼠模型。

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Nonalcoholic steatohepatitis (NASH) is a hepatic manifestation of the growing metabolic syndrome epidemic that could progress to cirrhosis. Animal models adequately mimicking this condition in humans are scanty. The objective of our study was to investigate whether high-fat diets (HFD) with adequate methionine and choline levels can induce pathophysiological features typical of human NASH in C57BL/6J mice. Forty C57BL/6J mice, divided into control and high-fat (HF) groups, were fed a low-fat diet or a HFD ad libitum, respectively, for 20 weeks. At the end of 20 weeks, animals were sacrificed and assays were performed for blood biomarkers typical of human NASH. Adipose tissue depots were collected and liver samples were processed for histological examination. High-fat feeding led to increased triglyceride accumulation in the liver (8.9 mumol/100 mg liver tissue vs. 2.6 mumol/100 mg for control) and induced histopathological features of human NASH including hepatic steatosis, ballooning inflammation and fibrosis. Expressions of proteins and chemokines predominant in NASH including collagens I, III and IV and platelet derived growth factor (PDGF) A and B were significantly higher in animals fed the HFD. Liver enzymes alanine transaminase, aspartate transaminase and alkaline phosphatase were significantly (P < 0.05) elevated in the HFD group compared to controls. Mice on HFD also developed hyperglycemia, hyperinsulinemia, hypoadiponectinemia along with elevated tumor necrosis factor alpha, resistin, leptin, free fatty acids, transforming growth factor beta and malondialdehyde levels that characterize NASH in humans. It is concluded that long-term HF feeding with adequate methionine and choline can induce many of the pathophysiological features typical of human NASH in C57BL/6J mice. All rights reserved, Elsevier.
机译：非酒精性脂肪性肝炎（NASH）是新陈代谢综合症流行病的肝病表现，可能发展为肝硬化。足以在人类中模仿这种状况的动物模型很少。我们研究的目的是研究具有适当蛋氨酸和胆碱水平的高脂饮食（HFD）是否可以诱导C57BL / 6J小鼠的典型NASH病理生理特征。分为对照组和高脂（HF）组的四十只C57BL / 6J小鼠分别接受低脂饮食或HFD随意喂养20周。在20周结束时，处死动物并进行人类NASH典型血液生物标志物的测定。收集脂肪组织贮库，并对肝脏样品进行组织学检查。高脂喂养导致肝脏中甘油三酸酯的积累增加（8.9摩尔/ 100毫克肝脏组织，而对照组则为2.6摩尔/ 100毫克），并诱导人NASH的组织病理学特征，包括肝脂肪变性，囊肿性炎症和纤维化。在喂食HFD的动物中，NASH中主要的蛋白质和趋化因子（包括胶原蛋白I，III和IV）以及血小板衍生生长因子（PDGF）A和B的表达明显较高。与对照组相比，HFD组的肝酶丙氨酸转氨酶，天冬氨酸转氨酶和碱性磷酸酶显着升高（ P <0.05）。 HFD小鼠还发展了高血糖，高胰岛素血症，低脂联素血症以及升高的肿瘤坏死因子α，抵抗素，瘦素，游离脂肪酸，转化生长因子β和丙二醛水平，这些是人类NASH的特征。结论是，长期HF喂养充足的蛋氨酸和胆碱可以诱导C57BL / 6J小鼠的许多典型NASH病理生理特征。保留所有权利，Elsevier。

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