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本文引用的文献

1
Significance of genetic polymorphisms in patients with nonalcoholic fatty liver disease.非酒精性脂肪性肝病患者基因多态性的意义
Clin J Gastroenterol. 2017 Jun;10(3):201-207. doi: 10.1007/s12328-017-0732-5. Epub 2017 Mar 13.
2
Non-alcoholic fatty liver disease - clinical and histopathological aspects.非酒精性脂肪性肝病——临床与组织病理学方面
Rom J Morphol Embryol. 2016;57(4):1295-1302.
3
Pathology of non-alcoholic fatty liver disease.非酒精性脂肪性肝病的病理学。
Liver Int. 2017 Jan;37 Suppl 1:85-89. doi: 10.1111/liv.13301.
4
Current evidence on the association of the metabolic syndrome and dietary patterns in a global perspective.从全球视角看代谢综合征与饮食模式的关联的现有证据。
Nutr Res Rev. 2016 Dec;29(2):152-162. doi: 10.1017/S095442241600007X.
5
A diet-induced Sprague-Dawley rat model of nonalcoholic steatohepatitis-related cirrhosis.非酒精性脂肪性肝炎相关性肝硬化的饮食诱导Sprague-Dawley大鼠模型。
J Nutr Biochem. 2017 Feb;40:62-69. doi: 10.1016/j.jnutbio.2016.10.007. Epub 2016 Oct 24.
6
High-fructose corn syrup-55 consumption alters hepatic lipid metabolism and promotes triglyceride accumulation.高果糖玉米糖浆-55 的摄入会改变肝脏的脂质代谢,促进甘油三酯的积累。
J Nutr Biochem. 2017 Jan;39:32-39. doi: 10.1016/j.jnutbio.2016.09.010. Epub 2016 Sep 30.
7
Animal models of non-alcoholic fatty liver disease: current perspectives and recent advances.非酒精性脂肪性肝病的动物模型:当前观点与最新进展
J Pathol. 2017 Jan;241(1):36-44. doi: 10.1002/path.4829. Epub 2016 Nov 22.
8
Inhibiting poly ADP-ribosylation increases fatty acid oxidation and protects against fatty liver disease.抑制多聚 ADP-核糖基化可增加脂肪酸氧化,预防脂肪肝疾病。
J Hepatol. 2017 Jan;66(1):132-141. doi: 10.1016/j.jhep.2016.08.024. Epub 2016 Sep 20.
9
Development of a Representative Mouse Model with Nonalcoholic Steatohepatitis.非酒精性脂肪性肝炎代表性小鼠模型的建立。
Curr Protoc Mouse Biol. 2016 Jun 1;6(2):201-210. doi: 10.1002/cpmo.1.
10
The Natural Course of Non-Alcoholic Fatty Liver Disease.非酒精性脂肪性肝病的自然病程。
Int J Mol Sci. 2016 May 20;17(5):774. doi: 10.3390/ijms17050774.

非酒精性脂肪性肝病饮食模式的最新进展:当前研究与见解

Updates on Dietary Models of Nonalcoholic Fatty Liver Disease: Current Studies and Insights.

作者信息

Stephenson Kristen, Kennedy Lindsey, Hargrove Laura, Demieville Jennifer, Thomson Joanne, Alpini Gianfranco, Francis Heather

机构信息

Scott & White Digestive Disease Research Center, Baylor Scott & White Health, Temple, TX, USA.

Research, Central Texas Veterans Health Care System, Temple, TX, USA.

出版信息

Gene Expr. 2018 Mar 21;18(1):5-17. doi: 10.3727/105221617X15093707969658. Epub 2017 Nov 2.

DOI:10.3727/105221617X15093707969658
PMID:29096730
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5860971/
Abstract

Nonalcoholic fatty liver disease (NAFLD) is a disease of increasing interest, as its prevalence is on the rise. NAFLD has been linked to metabolic syndrome, which is becoming more common due to the Western diet. Because NAFLD can lead to cirrhosis and related complications including hepatocellular carcinoma, the increasing prevalence is concerning, and medical therapy aimed at treating NAFLD is of great interest. Researchers studying the effects of medical therapy on NAFLD use dietary mouse models. The two main types of mouse model diets are the methionine- and choline-deficient (MCD) diet and the Western-like diet (WD). Although both induce NAFLD, the mechanisms are very different. We reviewed several studies conducted within the last 5 years that used MCD diet or WD mouse models in order to mimic this disease in a way most similar to humans. The MCD diet inconsistently induces NAFLD and fibrosis and does not completely induce metabolic syndrome. Thus, the clinical significance of the MCD diet is questionable. In contrast, WD mouse models consisting of high fat, cholesterol, and a combination of high-fructose corn syrup, sucrose, fructose, or glucose not only lead to metabolic syndrome but also induce NAFLD with fibrosis, making these choices most suitable for research.

摘要

非酒精性脂肪性肝病(NAFLD)是一种越来越受关注的疾病,因为其患病率正在上升。NAFLD与代谢综合征有关,由于西方饮食,代谢综合征正变得越来越普遍。由于NAFLD可导致肝硬化及包括肝细胞癌在内的相关并发症,其患病率的上升令人担忧,旨在治疗NAFLD的医学疗法备受关注。研究医学疗法对NAFLD影响的研究人员使用饮食小鼠模型。两种主要的小鼠模型饮食是蛋氨酸和胆碱缺乏(MCD)饮食和西式饮食(WD)。虽然两者都可诱发NAFLD,但其机制非常不同。我们回顾了过去5年中进行的几项研究,这些研究使用MCD饮食或WD小鼠模型,以便以最类似于人类的方式模拟这种疾病。MCD饮食诱发NAFLD和纤维化的情况不一致,并且不能完全诱发代谢综合征。因此,MCD饮食的临床意义值得怀疑。相比之下,由高脂肪、胆固醇以及高果糖玉米糖浆、蔗糖果糖或葡萄糖组合而成的WD小鼠模型不仅会导致代谢综合征,还会诱发伴有纤维化的NAFLD,这使得这些选择最适合用于研究。