[1]曹涵,曲伸.过氧化物酶体增殖物活化受体与非酒精性脂肪性肝病[J].国际内分泌代谢杂志,2014,(06):404-407.[doi:10.3760/cma.j.issn.1673-4157.2014.06.012]
 Cao Han,Qu Shen..Peroxisome proliferator-activated receptors and non-alcoholic fatty liver diseases[J].International Journal of Endocrinology and Metabolism,2014,(06):404-407.[doi:10.3760/cma.j.issn.1673-4157.2014.06.012]
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过氧化物酶体增殖物活化受体与非酒精性脂肪性肝病()
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《国际内分泌代谢杂志》[ISSN:1673-4157/CN:12-1383/R]

卷:
期数:
2014年06期
页码:
404-407
栏目:
综述
出版日期:
2014-12-20

文章信息/Info

Title:
Peroxisome proliferator-activated receptors and non-alcoholic fatty liver diseases
作者:
曹涵曲伸
200072 上海,同济大学附属第十人民医院内分泌代谢病科
Author(s):
Cao HanQu Shen.
Department of Endocrinology,Shanghai 10th People’s Hospital, Tongji University,Shanghai 200072,China
关键词:
过氧化物酶体增殖物活化受体 非酒精性脂肪性肝病 脂肪沉积
Keywords:
Peroxisome proliferators activated receptors Non-alcoholic fatty liver disease Fat accumulation
DOI:
10.3760/cma.j.issn.1673-4157.2014.06.012
摘要:
非酒精性脂肪性肝病(NAFLD)的发病率正在逐年升高,肝脏脂肪沉积是NAFLD的临床病理特征和诊断的金标准。过氧化物酶体增殖物活化受体(PPARs)是配体激活的核受体,在脂代谢、糖代谢和炎性反应中起关键作用,其可作为治疗NAFLD的靶点。PPARs激动剂可减少肝内脂肪沉积,从而逆转NALFD的发展进程,但因其尚存在较多不良反应,所以对PPARs与NAFLD的机制需要进一步研究,从而为PPARs治疗NAFLD提供更有力的证据。
Abstract:
The morbidity of non-alcoholic fatty liver disease(NAFLD)is increasing in recently decades. The hepatic steatosis is the main clinical pathological character and is used as the golden standard for the diagnosis of NAFLD. Peroxisome proliferators-activated receptors(PPARs)are ligand-activated nuclear receptors which regulate lipid and glucose metabolism as well as inflammation, and are therefore considered to be a therapeutic target of NAFLD. Studies showed that PPARs agonists reduced fat accumulation in the liver, thus reversing NAFLD progress. However,many side effects are noticed for PPARs agonists in the treatment of NAFLD, more studies are needed to improve our understanding of the roles of PPARs in the progress of NAFLD and find out new evidences for its usage in NAFLD.

参考文献/References:

[1] Guleria A,Duseja A,Kalra N,et al.Patients with non-alcoholic fatty liver disease(NAFLD)have an increased risk of atherosclerosis and cardiovascular disease[J].Trop Gastroenterol,2013,34(2):74-82.
[2] Monsalve FA,Pyarasani RD,Delgado-Lopez F, et al.Peroxisome proliferator-activated receptor targets for the treatment of metabolic diseases[J].Mediators Inflamm,2013(2013):549627.
[3] Fiévet C, Staels B. Efficacy of peroxisome proliferator-activated receptor agonists in diabetes and coronary artery disease[J].Curr Atheroscler Rep,2009,11(4):281-288.
[4] Lalloyer F,Staels B.Fibrates, glitazones, and peroxisome proliferator-activated receptors[J].Arterioscler Thromb Vasc Biol,2010,30(5):894-899.
[5] Staels B,Rubenstrunk A,Noel B, et al.Hepatoprotective effects of the dual peroxisome proliferator-activated receptor alpha/delta agonist, GFT505, in rodent models of nonalcoholic fatty liver disease/nonalcoholic steatohepatitis[J].Hepatology,2013,58(6):1941-1952.
[6] Chanda D,Lee CH,Kim YH, et al.Fenofibrate differentially regulates plasminogen activator inhibitor-1 gene expression via adenosine monophosphate-activated protein kinase-dependent induction of orphan nuclear receptor small heterodimer partner[J].Hepatology,2009,50(3):880-892.
[7] Fiorucci S,Antonelli E,Rizzo G, et al.The nuclear receptor SHP mediates inhibition of hepatic stellate cells by FXR and protects against liver fibrosis[J].Gastroenterology,2004,127(5):1497-1512.
[8] Bieghs V,Van Gorp PJ,Wouters K, et al.LDL receptor knock-out mice are a physiological model particularly vulnerable to study the onset of inflammation in non-alcoholic fatty liver disease[J].PLoS One,2012,7(1):e30668.
[9] Shiri-Sverdlov R,Wouters K,van Gorp PJ, et al.Early diet-induced non-alcoholic steatohepatitis in APOE2 knock-in mice and its prevention by fibrates[J].J Hepatol,2006,44(4):732-741.
[10] Linden MA,Fletcher JA,Morris EM, et al.Combining metformin and aerobic exercise training in the treatment of type 2 diabetes and NAFLD in OLETF rats[J].Am J Physiol Endocrinol Metab,2014,306(3):E300-E310.
[11] Hahm JR,Ahn JS,Noh HS, et al.Comparative analysis of fat and muscle proteins in fenofibrate-fed type Ⅱ diabetic OLETF rats: the fenofibrate-dependent expression of PEBP or C11orf59 protein[J].BMB Rep,2010,43(5):337-343.
[12] Cariou B,Zair Y,Staels B, et al.Effects of the new dual PPAR alpha/delta agonist GFT505 on lipid and glucose homeostasis in abdominally obese patients with combined dyslipidemia or impaired glucose metabolism[J].Diabetes Care,2011,34(9):2008-2014.
[13] Trottier J,Perreault M,Rudkowska I, et al.Profiling serum bile acid glucuronides in humans: gender divergences, genetic determinants, and response to fenofibrate[J].Clin Pharmacol Ther,2013,94(4):533-543.
[14] Wheeler MC,Gekakis N.Hsp90 modulates PPARγ activity in a mouse model of nonalcoholic fatty liver disease[J].J Lipid Res,2014,55(8):1702-1710.
[15] Zhang W,Wu R,Zhang F, et al.Thiazolidinediones improve hepatic fibrosis in rats with non-alcoholic steatohepatitis by activating the adenosine monophosphate-activated protein kinase signalling pathway[J].Clin Exp Pharmacol Physiol,2012,39(12):1026-1033.
[16] Zheng H,Li S,Ma L, et al.A novel agonist of PPAR-γ based on barbituric acid alleviates the development of non-alcoholic fatty liver disease by regulating adipocytokine expression and preventing insulin resistance[J].Eur J Pharmacol,2011,659(2-3):244-251.
[17] Yang L,Stimpson SA,Chen L, et al.Effectiveness of the PPARγ agonist, GW570, in liver fibrosis[J].Inflamm Res,2010,59(12):1061-1071.
[18] Kakiuchi-Kiyota S, Vetro JA, Suzuki S, et al. Effects of the PPARgamma agonist troglitazone on endothelial cells in vivo and in vitro: differences between human and mouse[J].Toxicol Appl Pharmacol,2009,237(1):83-90.
[19] Ratziu V,Charlotte F,Bernhardt C, et al.Long-term efficacy of rosiglitazone in nonalcoholic steatohepatitis: results of the fatty liver improvement by rosiglitazone therapy(FLIRT 2)extension trial[J].Hepatology,2010,51(2):445-453.
[20] Sathyanarayana P,Jogi M,Muthupillai R, et al.Effects of combined exenatide and pioglitazone therapy on hepatic fat content in type 2 diabetes[J].Obesity(Silver Spring),2011,19(12):2310-2315.
[21] Iwaisako K,Haimerl M,Paik YH, et al.Protection from liver fibrosis by a peroxisome proliferator-activated receptor δ agonist[J].Proc Natl Acad Sci U S A,2012,109(21):E1369-E1376.
[22] Barroso E,Astudillo AM,Balsinde J, et al.PPARβ/δ activation prevents hypertriglyceridemia caused by a high fat diet. involvement of AMPK and PGC-1α-Lipin1-PPARα pathway[J].Clin Investig Arterioscler,2013,25(2):63-73.
[23] Kostadinova R,Montagner A,Gouranton E, et al.GW501516-activated PPARβ/δ promotes liver fibrosis via p38-JNK MAPK-induced hepatic stellate cell proliferation[J].Cell Biosci,2012,2(1):34.
[24] Sahebkar A,Chew GT,Watts GF.New peroxisome proliferator-activated receptor agonists: potential treatments for atherogenic dyslipidemia and non-alcoholic fatty liver disease[J].Expert Opin Pharmacother,2014,15(4):493-503.
[25] Bays HE,Schwartz S,Littlejohn T, et al.MBX-8025, a novel peroxisome proliferator receptor-delta agonist: lipid and other metabolic effects in dyslipidemic overweight patients treated with and without atorvastatin[J].J Clin Endocrinol Metab,2011,96(9):2889-2897.
[26] Ban S, Kasuga JI, Nakagome I, et al. Structure-based design, synthesis, and nonalcoholic steatohepatitis(NASH)-preventive effect of phenylpropanoic acid peroxisome proliferator-activated receptor(PPAR)α-selective agonists[J].Bioorg Med Chem,2011,19(10):3183-3191.

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备注/Memo

备注/Memo:
基金项目:中华医学会临床医学科研专项基金(12020550355); 申康慢病综合防治项目(SHDC12012303)
更新日期/Last Update: 2014-12-20