Wapnir R A, Moak S A, Stiel L, Lifshitz F
Life Sci. 1982 Jun 28;30(26):2285-92. doi: 10.1016/0024-3205(82)90255-7.
A model of maternal lipemia without hyperglycemia, in the rat, produced by high-fat feedings, was developed to study the effects of and abnormal maternal lipid homeostasis on placental transport of nutrients and possible alterations of key enzymes of energy metabolism in the liver and brain of the fetuses. Pregnant rats fed lower concentrations of fat served as controls. All studies were carried out in dams and fetuses one day prior to delivery. The dietary treatment of the dams and fetuses produced in the fetuses ketonemia as well as lipemia. Following a bolus of 14C-3-0-methyl-D-glucose to the dams, the levels of the tracer remained higher in the blood and brain of lipemic than in control fetuses. By contrast, there was a decrease in the fluxes of 14C-alpha-amino-isobutyric acid in the fetuses of lipemic dams as compared to controls. Among enzymes of energy metabolism, fetal liver glucose-6-phosphatase and succinic dehydrogenase were enhanced by lipemia. Fetal brain glucose-6-phosphatase was depressed. Thus, lipemia, as occurring in poorly controlled maternal diabetes, may be a factor in determining the access to the fetus of essential, neutral amino acids and alter the normal activity of energy metabolism enzymes in the fetus.
通过高脂喂养建立了大鼠母体无高血糖的脂血症模型，以研究母体脂质稳态异常对胎盘营养物质转运以及胎儿肝脏和大脑中能量代谢关键酶可能改变的影响。喂食较低脂肪浓度的怀孕大鼠作为对照。所有研究均在分娩前一天对母鼠和胎儿进行。母鼠和胎儿的饮食处理在胎儿中产生了酮血症和脂血症。给母鼠注射大剂量的14C - 3 - O - 甲基 - D - 葡萄糖后，脂血胎儿血液和大脑中的示踪剂水平高于对照胎儿。相比之下，与对照相比，脂血母鼠胎儿中14C - α - 氨基异丁酸的通量降低。在能量代谢酶中，脂血症可增强胎儿肝脏葡萄糖 - 6 - 磷酸酶和琥珀酸脱氢酶。胎儿脑葡萄糖 - 6 - 磷酸酶受到抑制。因此，母体糖尿病控制不佳时出现的脂血症可能是决定必需中性氨基酸进入胎儿的一个因素，并改变胎儿能量代谢酶的正常活性。
