期刊文献+

PPARα,γ和δ:胰岛素抵抗治疗的靶点 被引量:10

PPARα,γ/δ:Potential Therapeutic Targets of Insulin Resistance
下载PDF
导出
摘要 胰岛素抵抗(insulin resistance,IR)是指外周组织对胰岛素的反应敏感性降低,是肝脏疾病和心血管病发生的共同基础,常常是高脂血症和2型糖尿病发病的前奏.过氧化物酶体增殖物激活受体(peroxisome proliferator-activated receptors,PPARs)属于核受体超家族的成员.PPARs激动剂可通过多种途径改善胰岛素敏感性,例如调节糖脂代谢、抗炎作用以及间接地改善氧化应激状态.这篇综述主要是回顾IR的病理机制及其治疗靶点:PPARα,δ和γ,并阐明针对此类靶点的胰岛素增敏药物的信号转导通路. Insulin resistance (IR) is manifested as the decreased response of the peripheral tissues to insulin. IR is an important pathophysiological mechanism in the development of hepatic diseases and cardiovascular disease. IR is also a preclinical indication of hyperlipemia and type 2 diabetes, where a variety of different molecular mechanisms are involved. The peroxisome proliferator-activated receptors (PPARs) are ligand-activated transcription factors belong to the nuclear receptor superfamily. PPARs agonists alleviate IR by regulating glucose and lipid metabolisms, including inhibition of inflammation and oxidative stress responses. In this review we discuss the pathogenesis of obesityinduced IR, focusing on its potential therapeutic targets: PPARα, γ and δ, as well as the related drugs with the signal transduction pathways to mediate their functions.
出处 《中国生物化学与分子生物学报》 CAS CSCD 北大核心 2014年第6期543-548,共6页 Chinese Journal of Biochemistry and Molecular Biology
基金 无锡市科技发展指导性计划(No.SCZ00N1133)资助~~
关键词 胰岛素抵抗 糖尿病 治疗靶点 过氧化物酶体增殖物激活受体 insulin resistance diabetes therapeutic targets peroxisome proliferator-activated receptors (PPARs)
  • 相关文献

参考文献2

二级参考文献44

  • 1Tontonoz P, Spiegelman B M. Fat and beyond: the diverse biology of PPARγ[J].Annu Rev Bioehem, 2008, 77 ( 1 ) :289-312.
  • 2Lehrke M, Lazar MA. The many faces of PPARγ [ J ]. Cell, 2005, 123 (6) : 993-999.
  • 3Wan Y. PPARγ in bone homeostasis [J]. Trends Endocrinol Metab,2010, 21(12) : 722-728.
  • 4Klotz L, Burgdoff S, Dani I, et al. The nuclear receptor PPAγ selectively inhibits Th17 differentiation in a T cell-intrinsic fashion and suppresses CNS autoimmunity [J].J Exp Med, 2009, 206( 10): 2079-2089.
  • 5Beekum O V, Fleskens V, Kalkhoven E. Posttranslational modifications of PPAR~,: fine-tuning the metabolic master regulator [J]. Obesity (Silver Spring) , 2009, 17(2) : 213-219.
  • 6Hu E, Kim J B, Sarraf P, et ul. Inhibition of adipogenesis through MAP kinase-mediated phosphorylation of PPARγ [J].Science, 1996,274 (5295) :2100-2103.
  • 7Gelman L, Michalik L, Desvergne B, et al. Kinase signaling cascades that modulate peroxisome proliferator-activated receptors [J]. Curt Opin Cell Biol, 2005, 17(2) : 216-222.
  • 8lankova I, Petersen RK, Annicotte J, et al. Peroxisome proliferator-activated receptor γ recruits the positive transcription elongation factor b complex to activate transcription and promote adipogenesis [ J]. Mol Endoeriaol, 2006, 20(7) : 1494-1505.
  • 9Compe E, Drane P, Laurent C, et al. Dysregulation of the peroxisome proliferator-activated receptor target genes by XPD mutations [ J]. Mol Cell Biol, 2005, 25(14) : 6065-6076.
  • 10Helenius K, Yang Y, Alasaari J, et al. Mat1 inhibits peroxisome proliferator-aetivated receptor "y-mediated adipoeyte differentiation [J]. Mol Cell Biol, 2009, 29(2) : 315-323.

共引文献2

同被引文献174

  • 1习雪峰,崔节荣,王勇.余甘子对胰岛素抵抗大鼠过氧化物酶体增生物激活受体γ表达的影响[J].食品科学,2009,30(5):253-256. 被引量:9
  • 2何新益,刘仲华.苦瓜多糖降血糖活性的高通量筛选研究[J].食品科学,2007,28(2):313-316. 被引量:29
  • 3刘毅,王文健,陈伟华,应健.黄芪多糖对3T3-L1前脂肪细胞增殖和分化的影响[J].中西医结合学报,2007,5(4):421-426. 被引量:40
  • 4刘芳芳,杨明炜,王晓强,王开富,陆付耳.梓醇与小檗碱及其配伍对胰岛素抵抗3T3-L1脂肪细胞的影响[J].中草药,2007,38(10):1523-1526. 被引量:16
  • 5MAHAPATRA D K, ASATI V, BHARTI S K. Chalcones and their therapeutic targets for the management of diabetes: structural and pharmacological perspectives[ J ]. Eur J Med Chem, 2015,92 ( 7 ) : 839-865.
  • 6MENENDEZ-GUTIERREZ M, ROSZER T, RICOTE M. Biology and therapeutic applications of peroxisome proliferator-activated receptors [ J]. Curr Top Med Chem,2012,12(6) :548-584.
  • 7CHIGURUPATI S, DHANARAJ S A, BALAKUMAR P. A step ahead of PPAR3' full agonists to PPAR'? partial agonists: therapeutic perspectives in the management of diabetic insulin resistance [ J ]. Eur J Pharmacol,2015,755( 1 ) :50-57.
  • 8LI Mindian, YANG Xiaoyong. A retrospective on nuclear receptor regulation of inflammation : lessons from GR and PPARs [ J ]. PPAR Res,2011,15(4) :742-785.
  • 9HUANG Huiyu, KORIVI M, YANG Huiting, et al. Effect of Pleurotus tuber-regium polysaecharides supplementation on the progression of diabetes complications in obese-diabetic rats[ J]. Chin J Physiol,2014,57(4) : 198-208.
  • 10BONFLEUR M L, BORCK P C, RIBEIRO R A, et al. Improvement in the expression of hepatic genes involved in fatty acid metabolism in obese rats supplemented with taurine[ J]. Life Sci ,2015,135:15- 21.

引证文献10

二级引证文献52

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部