摘要
目的:探讨高血糖及胰岛素不足对正常及糖尿病(DM)小鼠胃窦Cajal间质细胞(ICC)数量及超微结构的影响。方法:链脲佐菌素腹腔注射建立DM模型;分组:正常对照组(A组)、正常+高糖组(B组,予葡萄糖腹腔注射)、DM未干预组(C组)、DM+胰岛素组(D组,予长效胰岛素);监测血糖;饲养6周后ELISA测血清胰岛素,流式细胞法检测胃窦ICC数量,透射电镜观察ICC超微结构。结果:DM小鼠建模并干预6周后,与A组相比,B组血糖呈一过性增高,C组明显增高(P<0.05),D组无明显差异(P>0.05)。血清内源性胰岛素:B组与A组无显著差异;C、D组间也无显著差异(P>0.05),但均较A组低(P<0.05)。ICC数量:B组及DM各组均较A组减少(P<0.05),C组与D组无差异(P>0.05)。ICC超微结构:与A组比较,各实验组均可见:ICC细胞器溶解减少、线粒体空泡样变、细胞间隙增宽,尤以B、C组改变最突出。结论:DM小鼠胃窦ICC数量减少、伴有超微结构的改变;一过性及持续性高血糖主要使ICC超微结构严重破坏、数量也有减少;内源性胰岛素不足可能使ICC数量减少;但与ICC超微结构无明显相关,补充外源性胰岛素不能预防或阻止ICC数量改变,但可能通过降低高血糖而预防ICC细胞结构损害。
Objective： To investigate the effect of insulin and blood glucose interference on interstitial cells of Cajal （ICC） in normal and diabetes mellitus （DM） mice stomach antrum. Methods： DM model was established by intraperitoneal injection of streptozotocin （STZ） in C57/BL6 mice. A week later, all the normal and diabetic mice were randomly divided into 4 groups, group A（normal control） , B（normal mice administrated with high glucose）, C（diabetic mice without interference）, D（diabetic mice administrated with insulin）. The blood glucose of all the mice was tested once a week. Six weeks later, the level of serum insulin was detected by ELISA, the amount of ICC was detected by Flow cytometry （FCM） and the ultrastructure of ICC in stomach antrum was detected by transmission electron microscope （TEM）. Results： Compared with group A, there was a transient hyperglycemia in group B after injected glucose, and blood glucose in group C was significant inceased （P 〈 0.05）. But there was no significant difference in blood glucose level between group A and D （P 〉 0.05）. There was no significant difference in serum insulin level between group C or D,and no significant difference between group A and B （P 〉 0.05）.While compared with group A and B, serum insulin level in group C or D was significantly deceased （P 〈 0.05）. Compared with the group A, ICC quantity of the stomach centrum in B, C and D was significantly deceased （P 〈 0.05）. There was no significant difference in ICC quantity between group C and D （P 〉 0.05）. Compared with the group A, a significant ultrastructure change of ICC in group B, C and D was detected by TEM. The abnormal ultra-structure change of ICC in group B and C were most remarkable. Conclusions： There are quantitative decline and ultrastructure changes of ICC in DM mice stomach antrum. Both transient and persistence hyperglycemia may impair the ultrastructure of ICC and may cause ICC quantitative decline. Deficient of endogenous insulin may cause ICC quantitative decline, but not impair the ultrastructure of ICC directly. Add exogenous insulin can’t prevent from the quantity decline of ICC, but can prevent the ultrastructure change of ICC by controlling hyperglycemia.
出处
《南京医科大学学报（自然科学版）》
CAS
CSCD
北大核心
2008年第6期693-696,共4页
Journal of Nanjing Medical University(Natural Sciences)
基金
国家重点基础研究发展计划(2006CB503908)
关键词
血糖
胰岛素
糖尿病
胃窦
CAJAL间质细胞
blood glucose
insulin
diabetes mellitus
stomach antrum
interstitial cells of Cajal
