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本文引用的文献

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Rosiglitazone evaluated for cardiovascular outcomes--an interim analysis.罗格列酮心血管结局评估——一项中期分析。
N Engl J Med. 2007 Jul 5;357(1):28-38. doi: 10.1056/NEJMoa073394. Epub 2007 Jun 5.
2
Bezafibrate regulates the expression and enzyme activity of 11beta-hydroxysteroid dehydrogenase type 1 in murine adipose tissue and 3T3-L1 adipocytes.苯扎贝特调节小鼠脂肪组织和3T3-L1脂肪细胞中11β-羟基类固醇脱氢酶1型的表达和酶活性。
Am J Physiol Endocrinol Metab. 2007 Apr;292(4):E1213-22. doi: 10.1152/ajpendo.00340.2006. Epub 2006 Dec 26.
3
A placebo-controlled trial of pioglitazone in subjects with nonalcoholic steatohepatitis.一项关于吡格列酮治疗非酒精性脂肪性肝炎患者的安慰剂对照试验。
N Engl J Med. 2006 Nov 30;355(22):2297-307. doi: 10.1056/NEJMoa060326.
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Stearoyl-CoA desaturase-1 mediates the pro-lipogenic effects of dietary saturated fat.硬脂酰辅酶A去饱和酶-1介导膳食饱和脂肪的促脂肪生成作用。
J Biol Chem. 2007 Jan 26;282(4):2483-93. doi: 10.1074/jbc.M610158200. Epub 2006 Nov 23.
5
Prevalence of fatty liver in children and adolescents.儿童和青少年脂肪肝的患病率。
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Diabetes. 2006 Sep;55(9):2562-70. doi: 10.2337/db05-1322.
7
Fenofibrate, a peroxisome proliferator-activated receptor alpha agonist, reduces hepatic steatosis and lipid peroxidation in fatty liver Shionogi mice with hereditary fatty liver.非诺贝特是一种过氧化物酶体增殖物激活受体α激动剂,可减轻遗传性脂肪肝的Shionogi小鼠的肝脏脂肪变性和脂质过氧化。
Liver Int. 2006 Jun;26(5):613-20. doi: 10.1111/j.1478-3231.2006.01265.x.
8
Effect of multifactorial treatment on non-alcoholic fatty liver disease in metabolic syndrome: a randomised study.多因素治疗对代谢综合征中非酒精性脂肪性肝病的影响:一项随机研究。
Curr Med Res Opin. 2006 May;22(5):873-83. doi: 10.1185/030079906X104696.
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Effect of rosiglitazone on endothelial function and inflammatory markers in patients with the metabolic syndrome.罗格列酮对代谢综合征患者内皮功能和炎症标志物的影响。
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10
Prolonged n-3 polyunsaturated fatty acid supplementation ameliorates hepatic steatosis in patients with non-alcoholic fatty liver disease: a pilot study.长期补充n-3多不饱和脂肪酸可改善非酒精性脂肪性肝病患者的肝脂肪变性:一项初步研究。
Aliment Pharmacol Ther. 2006 Apr 15;23(8):1143-51. doi: 10.1111/j.1365-2036.2006.02885.x.

过氧化物酶体增殖物激活受体在非酒精性脂肪性肝病发病机制及治疗中的作用

Role of peroxisome proliferators-activated receptors in the pathogenesis and treatment of nonalcoholic fatty liver disease.

作者信息

Kallwitz Eric R, McLachlan Alan, Cotler Scott J

机构信息

Department of Medicine, University of Illinois, 840 S Wood Street, 7th Floor, MC 716, Chicago, IL 60612, USA.

出版信息

World J Gastroenterol. 2008 Jan 7;14(1):22-8. doi: 10.3748/wjg.14.22.

DOI:10.3748/wjg.14.22
PMID:18176957
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2673387/
Abstract

Nonalcoholic fatty liver disease (NAFLD) is highly prevalent and can result in nonalcoholic steatohepatitis (NASH) and progressive liver disease including cirrhosis and hepatocellular carcinoma. A growing body of literature implicates the peroxisome proliferators-activated receptors (PPARs) in the pathogenesis and treatment of NAFLD. These nuclear hormone receptors impact on hepatic triglyceride accumulation and insulin resistance. The aim of this review is to describe the data linking PPAR alpha and PPAR gamma to NAFLD/NASH and to discuss the use of PPAR ligands for the treatment of NASH.

摘要

非酒精性脂肪性肝病(NAFLD)非常普遍,可导致非酒精性脂肪性肝炎(NASH)以及包括肝硬化和肝细胞癌在内的进行性肝病。越来越多的文献表明,过氧化物酶体增殖物激活受体(PPARs)参与了NAFLD的发病机制和治疗。这些核激素受体影响肝脏甘油三酯的积累和胰岛素抵抗。本综述的目的是描述将PPARα和PPARγ与NAFLD/NASH联系起来的数据,并讨论使用PPAR配体治疗NASH的情况。