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首页> 外文期刊>Biology Open >Longitudinal characterization of diet-induced genetic murine models of non-alcoholic steatohepatitis with metabolic, histological, and transcriptomic hallmarks of human patients
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Longitudinal characterization of diet-induced genetic murine models of non-alcoholic steatohepatitis with metabolic, histological, and transcriptomic hallmarks of human patients

机译：饮食诱导的非酒精性脂肪性肝炎基因鼠模型的纵向表征，具有人类患者的代谢，组织学和转录组学特征

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Non-alcoholic steatohepatitis (NASH) is a fast-growing liver disease in the Western world. Currently, only a few animal models show both the metabolic and histological features of human NASH. We aimed to explore murine NASH models in a time dependent manner that exhibit metabolic, histological and transcriptomic hallmarks of human NASH. For this, the murine strains C57BL/6J, ob/ob, and KK-Aywere used and three types of nutritional regimes were administered: normal chow diet (NCD); high-fat, high-fructose, and high-cholesterol diet (fast food diet; FFD); or choline-deficient, L-amino acid-defined, high-fat diet (CDAHFD), for 2, 4, 8, 12, 18, 24, and 30?weeks. All strains under the FFD and CDAHFD regimes developed steatohepatitis. Among the strains treated with FFD, the non-alcoholic fatty liver disease (NAFLD) activity score, fibrosis progression and metabolic abnormalities such as hyperinsulinemia and obesity were more pronounced in ob/ob mice than in C57BL/6J and KK-Aymice. In ob/ob mice fed FFD, the development of hepatic crown-like structures was confirmed. Furthermore, molecular pathways involved in steatohepatitis and fibrosis showed significant changes from as early as 2?weeks of starting the FFD regime. Ob/ob mice fed FFD showed metabolic, histological, and transcriptomic dysfunctions similar to human NASH, suggesting their potential as an experimental model to discover novel drugs for NASH.
机译：非酒精性脂肪性肝炎（NASH）在西方世界是一种快速发展的肝病。目前，只有少数动物模型显示出人类NASH的代谢和组织学特征。我们旨在以时间依赖的方式探索鼠类NASH模型，该模型表现出人类NASH的代谢，组织学和转录组学特征。为此，使用了鼠类菌株C57BL / 6J，ob / ob和KK-Aywe，并施用了三种类型的营养方案：正常食物（NCD）;正常饮食（NCD）;正常饮食（NCD）。高脂，高果糖和高胆固醇饮食（快餐饮食; FFD）;或胆碱缺乏，L-氨基酸定义的高脂饮食（CDAHFD），持续2、4、8、12、18、24和30周。在FFD和CDAHFD体制下的所有菌株均发展为脂肪性肝炎。在用FFD处理的菌株中，ob / ob小鼠的非酒精性脂肪肝疾病（NAFLD）活性评分，纤维化进程和代谢异常（如高胰岛素血症和肥胖）比C57BL / 6J和KK-Aymice更明显。在喂食FFD的ob / ob小鼠中，证实了肝冠状结构的发育。此外，涉及脂肪变性肝炎和纤维化的分子途径从开始FFD方案的2周开始就显示出显着变化。喂食FFD的Ob / ob小鼠表现出与人NASH相似的代谢，组织学和转录组功能障碍，表明它们有潜力作为发现NASH新药的实验模型。

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