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PPARγ激动剂对糖尿病的肾脏保护作用 被引量：1

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摘要 过氧化物酶体增殖物激活受体(PPAR)γ激动剂具有多种生物效应。其中噻唑烷二酮类(TZDs)能够降低糖尿病大鼠和2型糖尿病患者尿微量白蛋白的排出,延缓糖尿病肾病的进展。一方面TZDs可通过降低血糖、血脂延缓糖尿病肾病的发展;另一方面还可直接诱导肾小球系膜细胞凋亡及抑制其增殖,抑制糖尿病肾病的发展。TZDs的肾脏保护机制可能独立于胰岛素增敏或降糖作用之外,而有二脂酰甘油(DAG)-蛋白激酶C(PKC)-细胞外信号调节激酶(ERK)和PKC-核因子(NF)-κB途径的参与。
作者 李慧 邹大进
机构地区 第二军医大学长海医院内分泌科
出处 《国外医学（内分泌学分册）》 2004年第2期105-107,共3页 Foreign Medical Sciences(Section of Endocrinology)
关键词 PPARΓ激动剂 糖尿病 生物效应 糖尿病肾病 血糖 血脂 系膜细胞
分类号 R587.1 [医药卫生—内分泌]
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参考文献25

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同被引文献5

  • 1Evans JL,Goldfine ID,Maddux BA,et al.Oxidative stress and stress-activited signaling pathway:a unifying hypothesis of type 2 diabetes.Endocrine Reviews,2002,23:599-622.
  • 2Catherwood MA,Powell LA,Anderson P,et al.Glucose-induced oxidative stress in mesangial cells.Kidney Int,2002,61:599-608.
  • 3Park CW,Kim JH,Lee JW,et al.High glucose-induced intercellular adhesion molecule-1(ICAM-1) expression through an osmotic effect in rat mesangial cells is PKC-NF-kB-dependent.Diabetologia,2000,43:1544-1553.
  • 4Sivarajah A,Chatteree PK,Patel NS,et al.Agonists of peroxisome-proliferator activated receptor-gamma reduce renal ischemia/reperfusion injury.Am J Nephrol,2003,23:267-276.
  • 5Bakris G,Viberti G,Weston WM,et al.Rosiglitazone reduces urinary albumin excretion in type 2 diabetes.J Human Hypertension,2003,17:7-12.

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国外医学（内分泌学分册）
2004年 第2期

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