期刊文献+

罗格列酮对不同糖耐量者的内皮障碍的影响 被引量:6

Endothelium dysfunction in subjects with various glucose tolerances and effect of rosiglitazone intervention
下载PDF
导出
摘要 目的探讨不同糖耐量者内皮障碍及罗格列酮对这一障碍的影响。方法应用罗格列酮(4mg/d,16周)治疗IFG、IGT及2型糖尿病病人并观察其对内皮损伤的标记物:尿白蛋白排泄率(UAER)、I型血浆纤溶酶原活化抑制剂(PAI-1)、假性血友病因子(vWF)、血浆血栓调节蛋白(TM)的影响。结果IFG、IGT及2型糖尿病的UAER、PAI-1、TM均较对照组明显增高(P<0.05或P<0.01)。2型糖尿病组的vWF较对照组明显增高(P<0.05)。2型糖尿病组的UAER、PAI-1、TM较IFG和IGT组也明显增高(P<0.05或P<0.01)。经罗格列酮治疗后UAER、PAI-1、vWF、TM水平呈不同程度的下降,且多具有显著意义。结论罗格列酮可以改善胰岛素抵抗所致的内皮功能障碍,对减少大血管病变的发生有积极的作用。 [Objective] To investigate the endothelium dysfunction in subjects with various glucose tolerances and the effect of rosiglitazone(RSG) intervention. [Methods] A total of subjects participated in the study were divided into four groups according to oral 75 g glucose tolerance test (OGTT). They were normal glucose tolerance (NGT) group, impaired fasting glucose(IFG), impaired glucose tolerance (IGT) and type 2 diabetes (T2DM) group. The patients of IFG, IGT and T2DM received 4 mg RSG daily for 16 weeks respectively. The markers of endothelium dysfunction including rates of urinary albumin excretion(UAER), Von willebrand factor(vWF), plasminogen activator inhibitor type-1(PAI-1), Thrombomodulin(TM)were detected. [Results] The levels of UAER, PAI-1, TM in IFG, IGT and T2DM groups were significantly higher than in NGT group (P <0.05 or P <0.01), the levels of vWF in T2DM group were significantly higher than in NGT group(P <0.05), and the levels of UAER, PAI-1, TM in T2DM group were significantly higher than in IFG and IGT groups (P <0.05 or P <0.01). Their levels were decreased to varying degrees after treatment with RSG for 16 weeks, and most of the decline were significant. [Conclusion] Rosiglitazone effectively suppresses the endothelium dysfunction of the patients of IFG, IGT and T2DM.
出处 《中国现代医学杂志》 CAS CSCD 北大核心 2005年第12期1844-1846,共3页 China Journal of Modern Medicine
基金 辽宁省教育厅基金项目(202013163)资助
关键词 罗格列酮 2型糖尿病 内皮细胞功能障碍 rosiglitazone type2 diabetes mellitus endothelium dysfunction
  • 相关文献

参考文献2

二级参考文献18

  • 1Smith U. Gogg S. Johansson A. et al. Thiazolidinediones(PPARγ)but not PPARα agnists increase IRS-2 gene expression in 3T3-L1 and human adipocytes. FASEB Journal, 2001,15:215-220.
  • 2Yong YL,Liang M.,Qi ZM. Experimental rat model of NIDDM.1990, 6(2): 115-116. Chinese
  • 3Kawano K, Hirashima T, Mori S, et al. Spontaneous long-term hyperglycemic rat with diabetic complications. Diabetes, 1992,41: 1422-1428.
  • 4Rui LY, Fisher TL. Thomas J, et al. Regulation of insulin/insulinlike growth factor-1 signaling by proteasome-mediated degradation of insulin receptor substrate-2 [J]. Journal of Biological Chemistry, 2001, 276(43): 40362-40367.
  • 5Lebrun P, Baron V, Hauck CR,et al. Cell adhesion and focal adhesion kinase regulate insulin receptor substrate-1 expression[J]. J Biol Chem, 2000, 275(49): 38371-38377.
  • 6Guang WL,Xiao RP, Stephen L,et al. A new insulin-sensitivity index for the population-based study [J]. Zhonghua Neike Zazhi,1993, 32(10): 656-660, Chinese
  • 7Shulman GI. Cellular mechanisms of insulin resistance[J]. J.Clin.Invest, 2000, 106(2): 171-176.
  • 8Pan ZA.Exploration to the relationship of dyslipidiaemia to the complications and prognosis of senile diabetes[J]. Zhongguo Xiandai Yixue Zazhi, 2003, 13(1): 61-63.
  • 9YAN C, Jinhong H. Dajin Zh. Insulin receptor substrate 2 and type 2 diabetes[J]. Guowai Yixue: Neifengmi Xuefengce, 2001,21(6): 291-293. Chinese
  • 10SUN XJ, WANG LM, ZHANG Y, et al. Role of IRS-2 in insulin and cytokine signaling[J]. Nature, 1995, 377: 173-177.

共引文献2126

同被引文献30

引证文献6

二级引证文献5

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