Diamant Y Z, Kissilevitz R, Shafrir E
Placenta. 1984 Jan-Feb;5(1):55-60. doi: 10.1016/s0143-4004(84)80048-x.
The activity of enzymes with a regulatory function in the pathways of glycolysis, gluconeogenesis and NADP-generation was investigated in 50 placentae from normal pregnancies and deliveries, 23 placentae from women with gestational diabetes, and 12 placentae from insulin-dependent patients. In placentae from the gestational diabetic group, the activity of pyruvate kinase and of NADPH-generating enzymes was raised and the activity of enzymes connected to glucogenesis was unchanged. These alterations were attributed to the oversupply of glucose and insulin to morphologically normal and well-oxygenated placental tissue. In the placentae from the insulin-dependent group, the activity of pyruvate kinase was reduced, the activity of NADPH-generating enzymes was enhanced and the activity of those related to the gluconeogenesis was unchanged. It is suggested that this pattern of enzyme changes reflects a reduction in the glycolytic capacity in these placentae, which may be due to inhibition by products of enhanced fatty acid oxidation in diabetes, amino acids and/or by long-term anoxia as a result of uteroplacental circulatory disturbances. The possible relation of reduced energy-forming capacity of the placenta in diabetes to its transport function is discussed.
在50例正常妊娠和分娩的胎盘、23例患有妊娠期糖尿病妇女的胎盘以及12例胰岛素依赖型患者的胎盘中,对糖酵解、糖异生和NADP生成途径中具有调节功能的酶的活性进行了研究。在妊娠期糖尿病组的胎盘中,丙酮酸激酶和NADPH生成酶的活性升高,而与糖异生相关的酶的活性未改变。这些改变归因于形态正常且氧合良好的胎盘组织中葡萄糖和胰岛素的供应过多。在胰岛素依赖型组的胎盘中,丙酮酸激酶的活性降低,NADPH生成酶的活性增强,与糖异生相关的酶的活性未改变。有人认为,这种酶变化模式反映了这些胎盘中糖酵解能力的降低,这可能是由于糖尿病中脂肪酸氧化增强的产物、氨基酸的抑制作用和/或由于子宫胎盘循环障碍导致的长期缺氧所致。文中讨论了糖尿病中胎盘能量形成能力降低与其转运功能之间的可能关系。