Effect of hyperinsulinemia on ovine fetal leucine kinetics during prolonged maternal fasting.
Effect of hyperinsulinemia on ovine fetal leucine kinetics during prolonged maternal fasting.
复制标题
长期母亲禁食期间高胰岛素血症对绵羊胎儿亮氨酸动力学的影响。
DOI：
10.1152/ajpendo.1992.263.4.e696
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发表时间：
1992
期刊：
影响因子：
--
通讯作者：
Denne,SC
中科院分区：
文献类型：
--
作者：
Liechty,EA;Boyle,DW;Moorehead,H;Liu,YM;Denne,SC
出生后胰岛素对全身蛋白质代谢的主要影响是减少蛋白质水解。为了评估胰岛素在产前蛋白质代谢调节中的作用，在基线和高胰岛素血症的反应中测定了绵羊胎儿的亮氨酸动力学。这些测量是在两种不同的母体状态下对每个胎儿进行的：自由喂养和母体禁食5天后。母体禁食导致胎儿亮氨酸出现率（Ra: 51.9 +/- 16.7 vs. 37.3 +/- 3.6 mumol/min, P < 0.05）和亮氨酸氧化率（Ra: 30.1 +/- 8.9 vs. 8.8 +/- 2.2 mumol/min, P < 0.05）显著增加。高胰岛素血症与胎儿葡萄糖利用显著增加相关，但不影响胎儿总亮氨酸R(a)或胎儿蛋白水解释放的亮氨酸。在营养充足的母体条件下，高胰岛素血症对胎儿氧化或非氧化处理亮氨酸没有影响。相比之下，在母体禁食期间，高胰岛素血症降低了胎儿亮氨酸氧化（11.0 +/- 3.7 vs. 31.1 +/- 8.9 mumol/min, P < 0.05），增加了亮氨酸的非氧化处理（35.4 +/- 4.0 vs. 19.0 +/- 6.1 mumol/min, P < 0.05）。这导致胎儿亮氨酸增加率由阴性变为阳性（-20.9 +/- 7.5 vs. 7.5 +/- 6.7 mumol/min, P < 0.05）。这些结果表明，在母体底物摄入受限的情况下，胎儿高胰岛素血症和随之而来的胎儿葡萄糖利用的增加与蛋白质合成的增加而不是蛋白质分解的减少有关，从而改善了胎儿亮氨酸胴体的增加。
The primary effect of insulin on whole body protein metabolism in postnatal life is to reduce proteolysis. To assess the role of insulin in the regulation of protein metabolism in prenatal life, leucine kinetics were determined in the ovine fetus at baseline and in response to hyperinsulinemia. These measurements were made in each fetus in two different maternal states: ad libitum maternal feeding and after a 5-day maternal fast. Maternal fasting resulted in significant increases in baseline fetal leucine rate of appearance (Ra; 51.9 +/- 16.7 vs. 37.3 +/- 3.6 mumol/min, P < 0.05) and leucine oxidation (30.1 +/- 8.9 vs. 8.8 +/- 2.2 mumol/min, P < 0.05). Hyperinsulinemia, which was associated with significant increases in fetal glucose utilization, did not affect total fetal leucine R(a) or leucine release from fetal proteolysis in either maternal state. Under well-fed maternal conditions, hyperinsulinemia produced no changes in the fetal oxidative or nonoxidative disposal of leucine. In contrast, during maternal fasting, hyperinsulinemia reduced fetal leucine oxidation (11.0 +/- 3.7 vs. 31.1 +/- 8.9 mumol/min, P < 0.05) and increased the nonoxidative disposal of leucine (35.4 +/- 4.0 vs. 19.0 +/- 6.1 mumol/min, P < 0.05). This resulted in a change in the fetal leucine accretion rate from negative to positive (-20.9 +/- 7.5 vs. 7.5 +/- 6.7 mumol/min, P < 0.05). These results suggest that, under conditions of restricted maternal substrate intake, fetal hyperinsulinemia and the attendant increase in fetal glucose utilization are associated with increased protein synthesis rather than decreased protein breakdown, thereby improving fetal leucine carcass accretion.