摘要
目的 : 观察膳食控制方法诱导的不同低硒动物模型胰岛代谢及功能的变化 ,进一步优化氧化侵袭与胰岛β细胞损害关系的动物模型研究。方法 : 分别应用天然、人工半合成低硒饲料、低硒附加一次大剂量注射 STZ、小剂量多次注射 STZ方法 ,诱导大鼠胰岛 β细胞损害模型 ,观察自由基代谢与胰岛 β细胞功能。结果 : 4种模型鼠不同程度地表现为全血和胰腺 GSH- Px活性显著低于非低硒组 ;血清 LPO与胰腺 MDA含量显著高于非低硒组 ;血清和胰腺组织胰岛素、C肽含量明显低于对照组。补充硒或 /和维生素 E组 ,血和胰腺 GSH- Px活性明显高于对照组 ;血清 LPO与胰腺 MDA含量则低于对照组 ;血清和胰腺组织胰岛素、C肽含量亦显著高于对照组。结论 : 4种动物模型中以低硒附加小剂量、多次注射 STZ诱导胰岛损害动物模型 。
Obejective: To investigate the islet functions and free radical metabolism of different Se-deficient rat models induced by diet control and chemical drugs and improve the animal model research of roles of oxidative stress in islet β cell lesions in nutritional field. Methods: The Se-deficient rat models and DM model on the basis of Se-deficient rats were made respectively with natural, artificial semisythetic diets, and the injection of streptozotocin into the Se-deficient rats. Both the free radical metabolism of pancreas and β cell functions in all rat mode ls were observed by biochemistry and radioimmunoassay. Results: T he decrease of GSH-Px, SOD activities and increase of LPO,MDA contents followed the decreased insulin level not only in serum but also in pancreas in almost all Se-deficient rat models. The supplementation of either Se or VE significantly decreased the contents of LPO, MDA and increased the insulin contents as well as the activities of antioxidant enzymes in serum and pancreas of the rats. Comclusion: The diabetes mellitus animal model induced on the basis of Se-deficient and by multiply and low doses injection of STZ is more useful for investigation of DM in nutritional fields.
出处
《营养学报》
CAS
CSCD
北大核心
2003年第4期409-413,共5页
Acta Nutrimenta Sinica
基金
国家自然科学基金(No.39870 6 6 7)
吉林省科委国际合作项目( No.2 0 0 2 0 70 4 )
吉林大学中日联谊医院重点项目基金
