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作 者:黄昶荃[1] 肖谦[1] 刘清秀[2] 赵柯湘[1] 牛桂芬[1] 李龙英[1]
机构地区:[1]重庆医科大学附属第一医院老年科,重庆400016 [2]绵阳市第三人民医院
出 处:《中国老年学杂志》2007年第5期406-408,共3页Chinese Journal of Gerontology
基 金:重庆市卫生局科技基金项目(项目编号:05-2-19)
摘 要:目的探讨胰岛素抵抗(IR)对心肌组织的损伤作用。方法6月龄Wistar大鼠,分为正常对照组和IR组,正常血糖胰岛素钳夹技术(EICT)测定各组大鼠IR,葡萄糖输注速率(GIR)表示IR情况;测量大鼠心脏重量(HW)和体重(BW)并计算心脏重量与体重之比(HW/BW);原位末端酶标记法(TUNEL)检测各组大鼠心肌细胞凋亡情况;观察心脏微细结构和心肌细胞超微结构;免疫组化检测心脏间质Ⅰ、Ⅲ型胶原水平。结果IR组大鼠GIR明显低于正常对照组(P<0.01),HW及HW/BW高于正常对照组,心肌细胞凋亡增多(P<0.01),GIR与心肌细胞凋亡指数呈负相关(r=-0.7452,P<0.05),心脏间质Ⅰ、Ⅲ型胶原水平增加(Ⅰ型胶原P<0.05,Ⅲ型胶原P<0.01);光镜和电镜可见IR组大鼠心肌组织发生损伤性改变。结论胰岛素抵抗可损伤心肌组织,导致心脏肥大、心肌细胞凋亡、心脏间质纤维化。Objective To investigate the injury effect of insulin resistance(IR) on cardiocyte and matrix in the rats with IR. Methods Wistar rats of 6 months old were randomly divided into normal control group ( N ) and IR group ( I ). Each group had eight rats. Euglycemic insulin clamp technique (EICT) was used to determine IR and glycose infusion rate(GIR) was used to IR. Cardiocyte apoptosis was evaluated by TUNEL. Heart weight(HW) and body weight(BW) were measured to calculate HW/BW. Fine structure of heart and ultramicrostructure of cardiocyte were observed. Collogen of Ⅰ ,Ⅲ type were evaluated by immunohistochemistry. Results Compared with controis, GIR decreased remarkably in I group(P 〈0.01 ). Content of Ⅰ ,Ⅲ type coUogen increased remarkably in I group , apoptosis cell number in the I group were higher than N group (P 〈0.01 ). In the rats with IR GIR showed a negative correlation with apoptosis cell number. Conclusions IR can cause hypertrophy of heart, cardiocyte apoptosis and myocardial interstitial fibrosis.
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