长期实验性应激对老龄、青龄糖尿病倾向鼠血糖影响的比较及其机制

目的:比较长期实验性应激源对老龄、青龄糖尿病倾向鼠血糖和胰岛素分泌的不同影响并探讨其机制。方法:取1-5 月龄( 青龄) 和15 月龄( 老龄) 昆明小鼠各40 只,用链脲佐菌素诱导糖尿病倾向后(STZ 鼠) ,各分为应激组与对照组。两组应激STZ 鼠均给予6 周实验性应激源刺激( 限制、旋转、拥挤) ,检测其空腹血糖(FBG) 、空腹血浆胰岛素(FINS) 、胰腺组织脂质过氧化物(LPO) 和一氧化氮代谢产物(NO-2 ,NO-3 ) 水平,观察胰腺组织超氧化物歧化酶(SOD) 活性的变化,并对STZ 鼠胰岛炎的严重程度进行评分。结果:经长期实验性应激的老龄STZ 鼠FBG 水平增高较青龄者显著,且FINS 水平明显下降;胰岛炎恶化较青龄STZ鼠严重;胰腺组织LPO 和NO-2 ,NO-3 含量增高及SOD 活性降低均较青龄STZ鼠明显;上述各指标间存在相关性。结论:长期实验性应激促使老龄STZ 鼠血糖增高、胰岛炎加重和胰岛素分泌机能耗竭的效应较青龄STZ 鼠明显;胰腺NO 过量及过氧化损伤可能参与这一差异的产生机制

Effect of long-term experimental stress on blood glucose level in mice with diabetes-prone: the age difference and its mechanism

Objective: To compare the effects of long term experimental stressors on blood glucose level and insulin secretion in the aged and young mice with diabetes prone and to explore the mechanism. Methods: Diabetes prone was induced by streptozotocin (STZ) in 40 1.5 month old mice and 40 15 month old mice. The young and the aged STZ mice were divided randomly into the stress group and the control group, respectively. Each group contained 20 mice. Both the aged and the young stress mice were exposed to multiple stressors (restrain, rotation, crowding) for 6 weeks. Fasting blood glucose (FBG), fasting plasma insulin (FINS), pancreas lipid peroxidate (LPO) and the metabolic products of nitric oxide (NO - 2, NO - 3) levels and superoxide dismutase (SOD) activity were measured. The grade of insulitis in STZ mice was also evaluated. Results: After 6 week stress, FBG level, pancreastissue LPO and NO - 2, NO - 3 contents were significantly higher while FINS level and SOD activity lower in the aged stress mice than those in the youngs. The insulitis malignization in the aged stress group was severer than that in the young stress group. There were correlativities among the above variables. Conclusion: The effects of long term stress in promoting hyperglycemia exacerbating insulitis, and inhibiting insulin secretion are more significant in the aged STZ mice than in the young ones. This difference may result from the excessive NO and the peroxide injury to the pancreas.