Hartmann K, Besch W, Zühlke H
Institute of Biochemistry, University of Greifswald, GDR.
Exp Clin Endocrinol. 1989 May;93(2-3):225-30. doi: 10.1055/s-0029-1210861.
With the aim of developing a model of experimental diabetes by which spontaneous recovery processes can be investigated, we used a lower (1) and a higher (2) dose of streptozotocin (SZ) to find out the lowest possible dose definitely inducing diabetes in mice through beta cell loss but preventing excessive damage to the endocrine pancreas which would exclude restoration processes. After application of SZ (1) to neonatal mice only male animals showed an overt diabetes in adult life. 70 percent of these mice had recovered 15 weeks after appearance of diabetes. Recovery was indicated by normalization of blood glucose, serum insulin, insulin secretion and biosynthesis of isolated pancreatic islets and a reenhancement of the pancreatic insulin content from lower than 10 to 30 percent of control values. After SZ (2) both sexes became hyperglycaemic, and the recovery rate was lower, but was increased by pregnancy in female mice. By means of this model it will be possible to investigate mechanisms and promoting factors of such restoration processes in more detail.
为了建立一个能够研究自发恢复过程的实验性糖尿病模型,我们使用了较低剂量(1)和较高剂量(2)的链脲佐菌素(SZ),以找出能通过β细胞损失在小鼠中明确诱导糖尿病,但又能防止对内分泌胰腺造成过度损伤从而排除恢复过程的最低可能剂量。将SZ(1)应用于新生小鼠后,只有雄性动物在成年后出现明显的糖尿病。这些小鼠中有70%在糖尿病出现后15周恢复。血糖、血清胰岛素、胰岛素分泌以及分离的胰岛的生物合成恢复正常,胰腺胰岛素含量从低于对照值的10%增加到30%,表明恢复。使用SZ(2)后,两性均出现高血糖,恢复率较低,但雌性小鼠怀孕后恢复率增加。通过这个模型,将有可能更详细地研究这种恢复过程的机制和促进因素。