Lin Y, Lee M, Leichter J
Division of Human Nutrition, University of British Columbia, Vancouver, Canada.
Teratog Carcinog Mutagen. 1995;15(3):147-53. doi: 10.1002/tcm.1770150307.
To determine the effect of maternal diabetes and alcohol intake, separately and in combination, on fetal growth and development, pregnant rats were divided into four groups: diabetic (D), diabetic plus alcohol (DA), control (C), and control plus alcohol (CA). Diabetes was induced by administration of streptozotocin before mating and alcohol was administered by gavage (2 g/kg body weight/day) on days 6-11 of gestation. Both diabetic groups (D and DA) had significantly lower weight gain during pregnancy compared to the controls (C and CA), despite the fact that the former consumed more food and water. Alcohol treatment resulted in reduced water and food intake and lower weight gain in the diabetic rats (DA), but not in the non-diabetic rats (CA), compared to their respective controls (D and C). On day 21 of gestation fetal body weights were significantly less and placental weights were significantly greater in the diabetic groups (D and DA) compared with the non-diabetic groups (C and CA). Differences in fetal and placental weights between rats exposed and not exposed to alcohol (C vs. CA and D vs. DA) were not significant. The number of fetuses with external malformations was significantly greater in the litters of alcohol exposed diabetic (DA) than non-alcohol exposed (D) animals. No external or skeletal malformations were observed in fetuses of non-diabetic rats regardless of whether or not they received alcohol (C or CA). The skeletal development of fetuses of diabetic rats, judged by the number and size of ossification centers on day 21 of gestation, was retarded when compared with fetuses of non-diabetic rats. Alcohol further retarded skeletal development of fetuses of diabetic animals (DA vs. D), but not of fetuses of non-diabetic rats (CA vs. C). It is concluded that maternal alcohol administration potentiates the effects of maternal diabetes on the incidence of fetal malformations and the retardation of skeletal development.
为了分别及联合确定母体糖尿病和酒精摄入对胎儿生长发育的影响，将怀孕大鼠分为四组：糖尿病组（D）、糖尿病加酒精组（DA）、对照组（C）和对照组加酒精组（CA）。在交配前通过注射链脲佐菌素诱导糖尿病，在妊娠第6至11天通过灌胃给予酒精（2克/千克体重/天）。尽管糖尿病组（D和DA）消耗的食物和水更多，但与对照组（C和CA）相比，这两组在怀孕期间体重增加明显更低。与各自的对照组（D和C）相比，酒精处理导致糖尿病大鼠（DA）的水和食物摄入量减少以及体重增加降低，但非糖尿病大鼠（CA）未出现这种情况。在妊娠第21天，与非糖尿病组（C和CA）相比，糖尿病组（D和DA）的胎儿体重明显更低，胎盘重量明显更高。暴露于酒精和未暴露于酒精的大鼠（C与CA以及D与DA）之间胎儿和胎盘重量的差异不显著。暴露于酒精的糖尿病（DA）动物窝中出现外部畸形的胎儿数量明显多于未暴露于酒精（D）的动物。无论是否接受酒精（C或CA），非糖尿病大鼠的胎儿均未观察到外部或骨骼畸形。与非糖尿病大鼠的胎儿相比，根据妊娠第21天骨化中心的数量和大小判断，糖尿病大鼠胎儿的骨骼发育延迟。酒精进一步延缓了糖尿病动物胎儿（DA与D）的骨骼发育，但未延缓非糖尿病大鼠胎儿（CA与C）的骨骼发育。得出的结论是，母体给予酒精会增强母体糖尿病对胎儿畸形发生率和骨骼发育迟缓的影响。
