Kaufmann R C, Khosho F K, Verhulst S J, Amankwah K S
Department of Obstetrics and Gynecology, Southern Illinois University School of Medicine, Springfield.
Am J Perinatol. 1991 Jan;8(1):11-4. doi: 10.1055/s-2007-999328.
Little is known about the effect of pregnancy on the 'BB' Wistar rat, an animal model of insulin-dependent (type I) diabetes. The pathogenesis of diabetes in this animal model seems to result from antibody-mediated natural killer cell destruction of pancreatic beta cells. The glucose metabolism of glucose intolerant female rats (study group) was studied prior to pregnancy, during pregnancy, and postpartum using glucose tolerance tests (GTT). Control rats with normal GTT were studied and bred in a fashion similar to the study animals. Before becoming pregnant, the GTT levels of the chemically diabetic rats were significantly different from those of the controls (p less than 0.05). The GTT values of the study animals decreased during pregnancy to levels seen in pregnant controls. After pregnancy, the GTT values of the study animals returned to prepregnant levels. Based on these observations, it appears that pregnancy may block the autoimmune destruction of beta cells, causing an increase in insulin production and release, thereby improving glucose metabolism.
关于妊娠对“BB”Wistar大鼠（一种胰岛素依赖型（I型）糖尿病动物模型）的影响，人们知之甚少。在这种动物模型中，糖尿病的发病机制似乎是由抗体介导的自然杀伤细胞对胰腺β细胞的破坏所致。使用葡萄糖耐量试验（GTT）对葡萄糖不耐受的雌性大鼠（研究组）在妊娠前、妊娠期间和产后的葡萄糖代谢进行了研究。对葡萄糖耐量试验正常的对照大鼠进行了研究，并以与研究动物相似的方式进行繁殖。在怀孕前，化学诱导糖尿病大鼠的葡萄糖耐量试验水平与对照组有显著差异（p小于0.05）。研究动物的葡萄糖耐量试验值在妊娠期间降至妊娠对照组的水平。妊娠后，研究动物的葡萄糖耐量试验值恢复到妊娠前水平。基于这些观察结果，似乎妊娠可能会阻断β细胞的自身免疫性破坏，导致胰岛素产生和释放增加，从而改善葡萄糖代谢。
