Leturque A, Hauguel S, Revelli J P, Burnol A F, Kandé J, Girard J
Centre de Recherches sur la Nutrition, Meudon-Bellevue, France.
Am J Physiol. 1989 Jun;256(6 Pt 1):E699-703. doi: 10.1152/ajpendo.1989.256.6.E699.
The effects of maternal hypoglycemia and/or hyperketonemia on glucose utilization by individual fetal rat tissues have been studied in vivo. To decrease blood glucose and to raise fetal blood ketone body concentrations, 19-day pregnant rats were submitted to 48 or 96 h of starvation. To differentiate between the effects of decreased blood glucose and increased ketone body concentrations, fed pregnant rats were infused for 2 h with DL-beta-hydroxybutyrate. After 96 h of maternal starvation, fetal 2-deoxy-D-glucose (2DG) uptake decreased from 13.6 +/- 0.5 to 8.6 +/- 1.15 micrograms.min-1.g-1. This was mainly due to a decrease in 2DG uptake by fetal hindlimb muscles and heart. By contrast, 2DG uptake in fetal liver and brain was not affected by maternal starvation. Acute hyperketonemia in fed pregnant rats induced a 23% decrease in 2DG uptake by the whole fetus mainly as the result of a lowered 2DG uptake in fetal hindlimb muscles. These data suggest that fetal 2DG uptake does not simply depend on lowered blood glucose level during maternal starvation but that other hormonal, cardiovascular, or metabolic adaptations are implicated. In the rat, most of the fetal tissues including brain are protected against maternal hypoglycemia.
在体内研究了母体低血糖和/或高酮血症对单个胎鼠组织葡萄糖利用的影响。为了降低血糖并提高胎儿血酮体浓度,对妊娠19天的大鼠进行48或96小时的饥饿处理。为了区分血糖降低和酮体浓度升高的影响,对喂食的妊娠大鼠输注DL-β-羟基丁酸2小时。母体饥饿96小时后,胎儿2-脱氧-D-葡萄糖(2DG)摄取量从13.6±0.5降至8.6±1.15微克·分钟-1·克-1。这主要是由于胎儿后肢肌肉和心脏对2DG的摄取减少。相比之下,胎儿肝脏和大脑中的2DG摄取不受母体饥饿的影响。喂食的妊娠大鼠急性高酮血症导致整个胎儿的2DG摄取减少23%,主要是由于胎儿后肢肌肉中2DG摄取降低所致。这些数据表明,胎儿2DG摄取并不简单地取决于母体饥饿期间血糖水平的降低,而是涉及其他激素、心血管或代谢适应性变化。在大鼠中,包括大脑在内的大多数胎儿组织都能免受母体低血糖的影响。