Prolonged maternal amino acid infusion in late-gestation pregnant sheep increases fetal amino acid oxidation.
Prolonged maternal amino acid infusion in late-gestation pregnant sheep increases fetal amino acid oxidation.
复制标题
妊娠晚期孕羊长时间输注母体氨基酸会增加胎儿氨基酸氧化。
DOI：
10.1152/ajpendo.00192.2009
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发表时间：
2009
期刊：
影响因子：
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通讯作者：
Brown,LauraD
中科院分区：
文献类型：
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作者：
Rozance,PaulJ;Crispo,MichelleM;Barry,JamesS;O'Meara,MeghanC;Frost,MackenzieS;Hansen,KentC;HayJr,WilliamW;Brown,LauraD
人类怀孕期间补充蛋白质不会改善胎儿生长，并可能增加小于胎龄儿的出生率和死亡率。为了确定可能的机制，双胎妊娠的绵羊在妊娠后期输注氨基酸（AA组，n = 7）或生理盐水（C组，n = 4）4天。AA组胎儿血浆亮氨酸、异亮氨酸、缬氨酸和赖氨酸浓度升高（P <0.05），苏氨酸浓度降低（P <0.05）。AA组胎儿动脉pH值（7.365 ± 0.007 d vs.血红蛋白-氧饱和度（46.2 ± 2.6vs.37.8 ± 3.6%，P <0.005）和总氧含量（3.17 ± 0.17vs.2.49 ± 0.20mmol/l，P <0.0001）在第4天较第0天降低。胎仔亮氨酸处置没有变化（9.22 ± 0.73 vs. 8.09 ± 0.63 μ mol·min-1·kg-1，AA vs. C），但AA组亮氨酸氧化速率增加43%（2.63 ± 0.16 vs. 1.84 ± 0.24 μ mol·min-1·kg-1，P <0.05）。AA组的胎儿氧利用率有增加的趋势（327 ± 23 vs. 250 ± 29 μ mol·min-1·kg-1，P = 0.06）。亮氨酸掺入胎儿蛋白的速率（5.19 ± 0.97 vs. 5.47 ± 0.89 μ mol·min-1·kg-1，AA vs. C）、蛋白质分解释放速率（4.20 ± 0.95 vs. 4.62 ± 0.74 μ mol·min-1·kg-1）和蛋白质增加速率（1.00 ± 0.30 vs. 0.85 ± 0.25 μ mol·min-1·kg-1）没有变化。与这些数据一致，胎儿骨骼肌泛素连接酶MaFBx 1或MuRF 1或蛋白质合成调节因子4E-BP 1、eEF 2、eIF2 α和p70 S6K均未发生变化。某些必需氨基酸浓度降低、氨基酸氧化增加、胎儿酸中毒和胎儿缺氧可能是解释母体补充氨基酸期间胎儿毒性的机制。
Protein supplementation during human pregnancy does not improve fetal growth and may increase small-for-gestational-age birth rates and mortality. To define possible mechanisms, sheep with twin pregnancies were infused with amino acids (AA group,n= 7) or saline (C group,n= 4) for 4 days during late gestation. In the AA group, fetal plasma leucine, isoleucine, valine, and lysine concentrations were increased (P< 0.05), and threonine was decreased (P< 0.05). In the AA group, fetal arterial pH (7.365 ± 0.007day 0vs. 7.336 ± 0.012day 4,P< 0.005), hemoglobin-oxygen saturation (46.2 ± 2.6 vs. 37.8 ± 3.6%,P< 0.005), and total oxygen content (3.17 ± 0.17 vs. 2.49 ± 0.20 mmol/l,P< 0.0001) were decreased onday 4compared withday 0. Fetal leucine disposal did not change (9.22 ± 0.73 vs. 8.09 ± 0.63 μmol·min−1·kg−1, AA vs. C), but the rate of leucine oxidation increased 43% in the AA group (2.63 ± 0.16 vs. 1.84 ± 0.24 μmol·min−1·kg−1,P< 0.05). Fetal oxygen utilization tended to be increased in the AA group (327 ± 23 vs. 250 ± 29 μmol·min−1·kg−1,P= 0.06). Rates of leucine incorporation into fetal protein (5.19 ± 0.97 vs. 5.47 ± 0.89 μmol·min−1·kg−1, AA vs. C), release from protein breakdown (4.20 ± 0.95 vs. 4.62 ± 0.74 μmol·min−1·kg−1), and protein accretion (1.00 ± 0.30 vs. 0.85 ± 0.25 μmol·min−1·kg−1) did not change. Consistent with these data, there was no change in the fetal skeletal muscle ubiquitin ligases MaFBx1 or MuRF1 or in the protein synthesis regulators 4E-BP1, eEF2, eIF2α, and p70S6K. Decreased concentrations of certain essential amino acids, increased amino acid oxidation, fetal acidosis, and fetal hypoxia are possible mechanisms to explain fetal toxicity during maternal amino acid supplementation.