茶多糖对糖尿病小鼠糖代谢、组织形态学及胰岛β细胞超微结构的影响

EFFECT OF TEA POLYSACCHARIDE ON GLUCOSE METABOLISM,HISTOMORPHOLOGY AND PANCREATIC ISLET BETA-CELL ULTRASTRUCTURE IN DIABETIC MICE

目的研究茶多糖(TP)对四氧嘧啶糖尿病小鼠糖代谢、组织形态学及胰岛β细胞超微结构的影响及其调节血糖的作用机制。方法将四氧嘧啶诱导的糖尿病小鼠随机分成4组对照组,低、中、高剂量TP组,每天分别灌胃给予蒸馏水、TP0.25、0.50、1.00g/(kgbw),连续5w,每周称重一次。在实验2w末、4w末各测空腹血糖一次。实验末期进行糖耐量实验;取股动脉血测血清胰岛素含量;取适量肝脏测肝糖元含量;制成10%肝匀浆测蛋白含量、己糖激酶(HK)、丙酮酸激酶(PK)活力;留取肝脏、胰腺、肾脏和脾脏做病理组织学检查;每组随机取5只小鼠胰腺做超薄切片、电镜观察。结果TP能明显缓解糖尿病小鼠症状;三个剂量组空腹血糖值均明显降低(P<0.05或P<0.01),糖耐量实验结果血糖曲线下面积下降,并存在剂量-反应关系。随着TP剂量的增高,血清胰岛素、肝糖元含量均明显增高,肝HK、PK活力均明显增强,以上各项指标均存在一定的剂量-反应关系。与对照组比,TP组肝细胞变性程度有所减轻,中、高剂量组肝组织病理变化总分均明显减少(P=0.000),胰岛数量明显恢复、体积增大,胰岛细胞明显修复、再生。三个剂量组小鼠胰岛数量明显高于对照组(P<0.05或P<0.01);胰岛β细胞内质网、线粒体等结构的损伤得到明显修复,酶原颗粒明显增多,细胞分泌等功能明显改善和恢复。结论TP能调节糖代谢,降低血糖,改善糖尿病小鼠的症状。

Objective To study tea polysaccharides （TP） on glucose metabolism, histopathology, and pancreatic islet β-cell ultrastructure in diabetic mice. Method The alloxan diabetic mice were randomly divided into 4 groups, and orally given distilled water, TP 0.25, 0.50, 1.00 g/（kg bw · d）. for 5 w, and weighed once every week. In experiment 2 and 4 w, the fasting blood glucose was tested once. The glucose tolerance test was conducted at the end of experiments. Blood serum insulin and liver glycogen were measured. The protein content, hexokinase （HK） and pyruvate kinase （PK） activity of 10% liver homogenate were measured. The histopathology of liver, pancreas, kidney and spleen tissue and the ultra structure of pancreas were observed. Results TP could significantly alleviate the symptoms of diabetic mice. The fasting blood glucose values in three TP groups were significantly decreased （P 〈0.05 or P〈0.01）, and glucose tolerance tests showed the area under curve decreased dose-dependently. As compared to the control group, the degree of liver cell degeneration was alleviated and the histopathological changes of liver tissue in medium and high dose TP groups were significantly less （P=0.000）, the number of pancreatic islets obviously restored, volume increased. The ultrastructural damage of β-cell endoplasmic reticulum and mitochondria was clearly restored, zymogen granules markedly increased, and the secretion of cells markedly improved and recovered in three TP groups than the control group （P 〈0.05 or P〈0.01）. Kidneys and spleen were not abnormally altered. Conclusion TP can regulate glucose metabolism, reduce blood sugar, and improve the symptoms in diabetic mice.