Girard J R, Ferré P, Gilbert M, Kervran A, Assan R, Marliss E B
Am J Physiol. 1977 May;232(5):E456-63. doi: 10.1152/ajpendo.1977.232.5.E456.
To determine the fetal response to altered maternal fuel supply, the effects of prolonged maternal fasting, begun 24-96 h before term, were examined and compared with values from normally fed term animals. Fetal weight decreased only after 48 h of maternal fasting. Prolonged maternal fasting was associated with low blood glucose, high blood ketone bodies, and decreased gluconeogenic substrate in the fetus. Plasma insulin was decreased, whereas plasma glucagon was increased in the fetus of fasted mothers. Infusion of [2-3H]glucose into the mother to constant specific activity gave a ratio of maternal to fetal glucose activity of 1.0 in fed and 1.56 in fasted mothers. Fetal liver from fasted mothers showed both increase in activity of key gluconeogenic enzymes (glucose-6-phosphatase and phosphoenolpyruvate carboxykinase) and increased conversion in vitro of lactate, alanine, serine, and glycerol in glucose by liver slices. It is inferred that maternal fasting induces fetal substrate alterations and hormonal changes appropriate to premature appearance of hepatic gluconeogenesis. The priority for endogenous fuel provision in this state leads to impaired fetal growth.
为了确定胎儿对母体燃料供应改变的反应，研究了在足月前24至96小时开始的母体长期禁食的影响，并与正常喂养的足月动物的值进行了比较。仅在母体禁食48小时后胎儿体重才下降。母体长期禁食与胎儿低血糖、高血酮体以及糖异生底物减少有关。禁食母亲的胎儿血浆胰岛素降低，而血浆胰高血糖素升高。以恒定比活性向母体输注[2-³H]葡萄糖，在喂食的母亲中母体与胎儿葡萄糖活性的比率为1.0，在禁食的母亲中为1.56。禁食母亲的胎儿肝脏显示关键糖异生酶（葡萄糖-6-磷酸酶和磷酸烯醇丙酮酸羧激酶）的活性增加，并且肝脏切片在体外将乳酸、丙氨酸、丝氨酸和甘油转化为葡萄糖的能力增强。据推测，母体禁食会诱导胎儿底物改变和激素变化，以适应肝糖异生过早出现。在这种状态下内源性燃料供应的优先级导致胎儿生长受损。
