Felig P, Kim Y J, Lynch V, Hendler R
J Clin Invest. 1972 May;51(5):1195-202. doi: 10.1172/JCI106913.
To evaluate the factors regulating gluconeogenesis in pregnancy, plasma amino acid levels were determined during the course of an 84-90 hr fast in physically healthy women studied during wk 16-22 of gestation (before undergoing therapeutic abortion), and in nonpregnant controls. The effect of pregnancy on the glycemic response to exogenous alanine administration during starvation was also investigated. In the nonpregnant group fasting resulted in a 2- to 3-fold increase in the levels of plasma valine, leucine, isoleucine, and alpha-aminobutyrate, while the concentration of alanine and glycine fell. In the pregnant group, the levels of most amino acids were significantly reduced in the postabsorptive state. With starvation, the plasma concentration of alanine fell more rapidly in the pregnant group and was significantly below that of the nonpregnant subjects for the first 60 hr of the fast. In contrast, a significant elevation in plasma glycine, serine, and threonine was observed in the pregnant group after 84 hr of fasting, whereas similar increments were not demonstrable until after 10 days of fasting in previously studied nonpregnant obese subjects. Paralleling the changes in maternal plasma, amniotic fluid levels of valine, leucine, and isoleucine increased while that of alanine fell during the fast. Although the plasma glucose concentration was lower in the pregnant group at termination of the fast, intravenous alanine administration (0.15 g/kg), resulted in a prompt, comparable increase (20-25 mg/100 ml) in plasma glucose in both groups of subjects. It is concluded that (a) pregnancy accelerates and exaggerates the hypoalaninemic and hyperglycinemic effects of starvation; (b) lack of key endogenous substrate rather than altered intrahepatic processes may limit hepatic gluconeogenesis in pregnancy and contribute to gestational hypoglycemia; (c) maternal caloric deprivation profoundly alters the levels of amino acids in amniotic fluid.
为评估孕期糖异生的调节因素,对妊娠16 - 22周(接受治疗性流产前)身体健康的孕妇及非孕对照者进行了84 - 90小时禁食期间血浆氨基酸水平的测定。同时还研究了妊娠对饥饿期间外源性丙氨酸给药血糖反应的影响。在非孕组,禁食导致血浆缬氨酸、亮氨酸、异亮氨酸和α -氨基丁酸水平升高2至3倍,而丙氨酸和甘氨酸浓度下降。在孕组,大多数氨基酸在吸收后状态下显著降低。饥饿时,孕组丙氨酸血浆浓度下降更快,在禁食的前60小时显著低于非孕受试者。相反,孕组禁食84小时后血浆甘氨酸、丝氨酸和苏氨酸显著升高,而在先前研究的非孕肥胖受试者中,类似的升高直到禁食10天后才出现。与母体血浆变化平行,禁食期间羊水缬氨酸、亮氨酸和异亮氨酸水平升高,而丙氨酸水平下降。尽管禁食结束时孕组血浆葡萄糖浓度较低,但静脉注射丙氨酸(0.15 g/kg)后,两组受试者血浆葡萄糖均迅速出现相当程度的升高(20 - 25 mg/100 ml)。结论如下:(a)妊娠加速并加剧了饥饿的低丙氨酸血症和高甘氨酸血症效应;(b)关键内源性底物的缺乏而非肝内过程的改变可能限制孕期肝糖异生并导致妊娠低血糖;(c)母体热量剥夺深刻改变了羊水中氨基酸的水平。