Mende S, Mühle W, Peters W H
Institute of Clinical Chemistry, University of Greifswald, Germany.
Horm Metab Res. 1996 Feb;28(2):81-5. doi: 10.1055/s-2007-979133.
Wistar rats with non-insulin dependent diabetes induced by neonatal streptozotocin (STZ) administration were raised either in large or in small litters. The STZ-treated rats from small litters showed a higher body weight as well as increased blood glucose levels compared with vehicle- and STZ-treated rats reared in large nests at an age of 8 weeks. The higher body weight of these rats was maintained until an age of 15 weeks, whereas the basal blood glucose was normalized. However, both STZ-treated groups exhibited an impaired glucose tolerance. During pregnancy only the glucose tolerance of the STZ-treated animals from large nests was improved although not normalized. The STZ-treated rats from small nests failed to adapt to pregnancy because the blood glucose levels after glucose load were similar to values found in the virgin state. The body weight of pregnant STZ treated rats raised in small litters was significantly lower than in vehicle- or STZ-terated rats from large nests. The number of fetuses per litter was similar in all groups tested. Compared with the vehicle-treated rats from large litters the fetal body weight of STZ-treated rats from small nests was decreased and that of STZ rats raised in large litters was increased. These results suggest that the rats with the more impaired glucose tolerance produce growth-retarded pups and, conversely, rats with rather mild impairment have bigger fetuses than the vehicle-treated ones. In the present study we have examined for the first time the combined effects of postnatal overnutrition and pregnancy on glucose homeostasis of rats treated neonatally with STZ. Our data demonstrate that postnatal overnutrition is an aggravating factor in the development of a diabetic state in these rats, especially at times when the insulin requirement is higher such as puberty and pregnancy.
通过新生期注射链脲佐菌素（STZ）诱导产生非胰岛素依赖型糖尿病的Wistar大鼠，分别饲养于大小不同的窝中。与8周龄时饲养在大窝中的溶媒对照组和STZ处理组大鼠相比，饲养在小窝中的STZ处理组大鼠体重更高，血糖水平也更高。这些大鼠较高的体重一直维持到15周龄，而基础血糖恢复正常。然而，两个STZ处理组的葡萄糖耐量均受损。在孕期，只有饲养在大窝中的STZ处理动物的葡萄糖耐量得到改善，尽管未恢复正常。饲养在小窝中的STZ处理大鼠未能适应妊娠，因为葡萄糖负荷后的血糖水平与未孕状态时的值相似。饲养在小窝中的妊娠STZ处理大鼠的体重显著低于饲养在大窝中的溶媒对照组或STZ处理组大鼠。所有测试组每窝胎儿数量相似。与饲养在大窝中的溶媒对照组大鼠相比，饲养在小窝中的STZ处理大鼠的胎儿体重降低，而饲养在大窝中的STZ大鼠的胎儿体重增加。这些结果表明，葡萄糖耐量受损更严重的大鼠产出的幼崽生长发育迟缓，相反，受损程度相对较轻的大鼠的胎儿比溶媒对照组的胎儿更大。在本研究中，我们首次研究了出生后营养过剩和妊娠对新生期用STZ处理的大鼠葡萄糖稳态的联合影响。我们的数据表明，出生后营养过剩是这些大鼠糖尿病状态发展的一个加重因素，尤其是在胰岛素需求较高的时期，如青春期和孕期。
