高胰岛素血症、高脂血症致动脉粥样硬化的实验研究  

An experimental study of hyperinsulinemia and hyperlipidemia on the pathogenesis of atherosclerosis

作　　者：沈捷[1] 刘铨之[1] 陈家伟[1] 周大虎[2] 薛婉芬[2] 

机构地区：[1]南京医科大学第一附院内分泌科,210029 [2]南京医科大学基础医学院

出　　处：《中国糖尿病杂志》1998年第2期97-100,共4页Chinese Journal of Diabetes

摘　　要：使用加与不加高脂血清的不同浓度胰岛素对培养的动脉平滑肌细胞进行刺激，以了解其光学及电镜结构改变。结果显示：胰岛素促细胞生长强度与胰岛素浓度成正比，高脂血清使平滑肌细胞排列无序化，失去特征结构，变为泡沫细胞；胰岛素与高脂血清复合作用，不仅使细胞形态、结构改变，并使之由收缩型变为增殖型，还导致胶原纤维产生。结果提示：控制高胰岛素血症、高脂血症患者的血胰岛素、血脂水平，有助于预防和推迟动脉粥样硬化的产生和发展。The proliferation and cytomorphological changes of SMC play important role in the pathogenesis of atherosclerosis (AS). The observations of cultured rabbit arterial SMC in media containing insulin 10uU, 1000uU and 10000uU/ml with and without 5 % hyperlipidmic serum(HLS) by LM and TEM were carried out. The results were as follows: ① Insulin without HLS stimulated the proliferation of SMC:the stimulatory effect on the proliferation of SMC seemed to be stronger with increasing concentrations of insulin but no morphological changes were shown in the shape and arrangement of SMC;② HLS caused direct effect on SMC by leading to the loss of myofibrils and dense bodies,modifying its shape from spindle to oval or round form,and converting SMC to foam cells: ③ Insulin with HLS not only modified the shape of SMC but also changed the phenotypic state from the contractile to the synthetic state. Insulin with HLS enhanced the production of collagen. All the above mentioned changes of SMC could be seen in atherogenesis,and hyperinsulinemia associated with hyperlipidemia enhanced the development of AS. Our results suggest that it is rational to normalize both the insulin level and dyslipidemia in order to prevent or delay the premature development of AS.

关 键 词：高胰岛素血症 高脂血清 动脉粥样硬化 实验 

分 类 号：R543.5[医药卫生—心血管疾病]