Veselá J, Rehák P, Baran V, Koppel J
Institute of Animal Physiology, Slovak Academy of Sciences, Kosice.
J Reprod Fertil. 1994 Mar;100(2):561-5. doi: 10.1530/jrf.0.1000561.
Female mice were injected with a single dose of streptozotocin (65 mg kg-1) 14-17 days before fertilization to investigate the significance of impaired insulin secretion induced by subdiabetic streptozotocin treatment on preimplantation embryo development. Subdiabetic mice (streptozotocin-treated) had significantly different glucose tolerance from that of control animals, despite similar basal glycaemia. Morphological analysis of preimplantation embryos collected on day 2 of pregnancy revealed no significant changes in the number of two-cell embryos recovered from streptozotocin-treated females compared with controls. Two-cell embryos were transferred into the oviducts of healthy, synchronous pseudopregnant females and recovered 24-28 h later. Morphological evaluation revealed a significantly greater percentage of degenerated embryos from streptozotocin-treated females than from control females. Morphological analysis of preimplantation embryos collected on day 2.5 of pregnancy revealed no significant changes in the number of two- to four-cell embryos recovered from streptozotocin-treated females compared with controls, but there was a significant increase in the number of degenerated embryos in streptozotocin-treated females that did not receive insulin therapy. Insulin (1-1.5 iu per 100 g) administered twice a day to streptozotocin-treated mice significantly improved the altered development of embryos in both experiments. It is possible that the impaired insulin secretion in female mice adversely affected the growth of preimplantation embryos. Almost half of the morphologically normal two-cell embryos isolated from subdiabetic females were incapable of development to the eight-cell stage even in a non-diabetic maternal environment. the morphologically distinct degenerative changes were first detected at the time of the second mitotic cleavage.
在受精前14 - 17天给雌性小鼠注射单剂量链脲佐菌素(65毫克/千克),以研究亚糖尿病剂量链脲佐菌素治疗诱导的胰岛素分泌受损对植入前胚胎发育的影响。尽管基础血糖水平相似,但亚糖尿病小鼠(链脲佐菌素治疗组)的糖耐量与对照动物有显著差异。对妊娠第2天收集的植入前胚胎进行形态学分析发现,与对照组相比,链脲佐菌素治疗的雌性小鼠回收的二细胞胚胎数量没有显著变化。将二细胞胚胎转移到健康、同期假孕雌性小鼠的输卵管中,24 - 28小时后回收。形态学评估显示,链脲佐菌素治疗的雌性小鼠的退化胚胎百分比显著高于对照雌性小鼠。对妊娠第2.5天收集的植入前胚胎进行形态学分析发现,与对照组相比,链脲佐菌素治疗的雌性小鼠回收的二至四细胞胚胎数量没有显著变化,但未接受胰岛素治疗的链脲佐菌素治疗的雌性小鼠中退化胚胎的数量显著增加。在两个实验中,每天给链脲佐菌素治疗的小鼠注射两次胰岛素(每100克1 - 1.5国际单位)可显著改善胚胎发育的改变。雌性小鼠胰岛素分泌受损可能对植入前胚胎的生长产生不利影响。即使在非糖尿病的母体环境中,从亚糖尿病雌性小鼠分离出的形态正常的二细胞胚胎中,几乎有一半无法发育到八细胞阶段。形态学上明显的退化变化首先在第二次有丝分裂时被检测到。