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罗格列酮对胰岛素抵抗大鼠β细胞作用形态学观察 被引量:1

Morphologic observation of the effect of rosiglitazone on β cells in insulin-resistant rats
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摘要 目的 研究罗格列酮 (RSG)对胰岛素抵抗 (IR)大鼠 β细胞超微结构病变的作用。 方法高糖饲料喂养SD大鼠 6周复制IR大鼠模型。成模后用药组予RSG 10 μmol·kg-1·d-1,用药 6周。未用药IR大鼠模型为对照 (IR组 )。透射电镜观察胰岛 β细胞超微结构。 结果 与IR组相比 ,RSG组大鼠收缩压、血清甘油三酯、游离脂肪酸、胰岛素降低 (均P <0 .0 1) ,胰岛素敏感指数、血清高密度脂蛋白胆固醇升高 (均P <0 .0 1)。电镜观察IR大鼠 β细胞可见凋亡早期改变 ,细胞浆内脂质沉积以及细胞核和细胞器的病理变化。RSG组 β细胞超微结构病变明显减轻 ,未见凋亡的 β细胞及胞浆内脂质沉积。 结论 罗格列酮可有效防治高糖饲料诱导IR大鼠 Objective To study the effect of rosiglitazone on pathologic changes of β cell ultrastructure in insulin-resistant (IR) rats. Methods IR rat model was established in 6-8-week-old SD rats by high-glucose feeding (70% calories from glucose) for 6 weeks. The IR rats was then divided into IR group (n=10) and rosiglitazone (RSG) group (n=10). Rats in RSG group were treated with RSG 10 μmol·kg -1·d -1 for 6 weeks by gavage. Ultrastructure of β cells was observed with transmission electron microscope. Results Systolic blood pressure and serum levels of triglyceride, free fatty acids and insulin in RSG group were lower than those in IR group (all P<0.01). Serum high density lipoprotein cholesterol and insulin sensitivity index were higher in RSG group than those in IR group (both P<0.01). The β cells in IR group showed early apoptosis, fat accumulation in cytoplasm as well as pathologic changes in nuclei and organelles. Pathologic changes in nuclei and organelles of β cells in RSG group were significantly attenuated. The β cells in RSG group did not show apoptosis and fat accumulation in cytoplasm. Conclusion RSG can effectively protect β cells from damage in high glucose-induced IR rats.
出处 《中华内分泌代谢杂志》 CAS CSCD 北大核心 2004年第3期203-205,共3页 Chinese Journal of Endocrinology and Metabolism
基金 上海市卫生局医学发展基金重点项目〔2 0 0 1ZD0 0 2 (3)〕
关键词 罗格列酮 胰岛素抵抗 大鼠 Β细胞 形态学观察 超微结构 Rosiglitazone Insulin resistance Islet β cells Ultrastructure
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参考文献10

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共引文献9

同被引文献2

  • 1M. Dubois,F. Pattou,J. Kerr-Conte,V. Gmyr,B. Vandewalle,P. Desreumaux,J. Auwerx,K. Schoonjans,J. Lefebvre. Expression of peroxisome proliferator-activated receptor γ (PPARγ) in normal human pancreatic islet cells[J] 2000,Diabetologia(9):1165~1169
  • 2J. W. M. H?ppener,C. Oosterwijk,M. G. Nieuwenhuis,G. Posthuma,J. H. H. Thijssen,Th. M. Vroom,B. Ahrén,C. J. M. Lips. Extensive islet amyloid formation is induced by development of Type II diabetes mellitus and contributes to its progression: pathogenesis of diabetes in a mouse model[J] 1999,Diabetologia(4):427~434

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