Kliegman R M, Morton S
Department of Pediatrics, Case Western Reserve University, Rainbow Babies and Children's Hospital, Cleveland, Ohio 44106.
Pediatr Res. 1988 Sep;24(3):302-7. doi: 10.1203/00006450-198809000-00005.
We determined metabolic responses after enteric galactose alimentation in 5- to 7-day-old newborn rats fasted for 24 h. The glycemic response was attenuated after enteric galactose feeding compared with the response after enteric glucose-fed rat pups. 14C radioactivity in blood from galactose-fed pups was reduced as counts in blood galactose were lower than counts in blood glucose in glucose-fed pups. Nonetheless within 15 min, [14C] from galactose appeared in blood glucose suggesting rapid conversion of galactose to glucose. The plasma insulin response was also attenuated after galactose feeding compared with the insulin response after enteric glucose. Hepatic glycogen content increased rapidly after enteric galactose feeding and was higher than after glucose feeding at 60, 120, and 180 min. Significant glycogen synthesis after oral glucose was delayed and occurred at 240 min. Carbon radioactivity in glycogen was higher in galactose fed pups between 15 and 360 min of the study. Serial determination of hepatic metabolites revealed an increase of galactose-1-phosphate levels after oral galactose at 240 and 300 min and a transient decline of ATP at 15 min. Other hepatic metabolites did not demonstrate significant differences between the two groups. These data suggest that hepatic glycogen synthesis is more rapid and occurs sooner after galactose than after glucose alimentation in previously fasted newborn rats. Galactose may enter a more direct pathway for neonatal hepatic glycogen synthesis. The relatively delayed entry of glucose label into hepatic glycogen and the delay of net glycogen synthesis after oral glucose suggest that glucose entry is not direct and may require further metabolism before incorporation into glycogen.(ABSTRACT TRUNCATED AT 250 WORDS)
我们测定了禁食24小时的5至7日龄新生大鼠经肠道给予半乳糖后的代谢反应。与经肠道给予葡萄糖的幼鼠相比，经肠道给予半乳糖后血糖反应减弱。半乳糖喂养幼鼠血液中的14C放射性降低，因为半乳糖喂养幼鼠血液中的计数低于葡萄糖喂养幼鼠血液中的葡萄糖计数。尽管如此，在15分钟内，半乳糖中的[14C]出现在血糖中，表明半乳糖迅速转化为葡萄糖。与经肠道给予葡萄糖后的胰岛素反应相比，给予半乳糖后血浆胰岛素反应也减弱。经肠道给予半乳糖后肝糖原含量迅速增加，在60、120和180分钟时高于给予葡萄糖后。口服葡萄糖后显著的糖原合成延迟，在240分钟时发生。在研究的15至360分钟内，半乳糖喂养幼鼠糖原中的碳放射性更高。肝脏代谢物的系列测定显示，口服半乳糖后240和300分钟时1-磷酸半乳糖水平升高，15分钟时ATP短暂下降。两组之间其他肝脏代谢物没有显著差异。这些数据表明，在先前禁食的新生大鼠中，肝糖原合成在给予半乳糖后比给予葡萄糖后更快且更早发生。半乳糖可能进入更直接的新生儿肝糖原合成途径。葡萄糖标记物进入肝糖原相对延迟以及口服葡萄糖后净糖原合成延迟表明葡萄糖进入不是直接的，可能需要进一步代谢才能掺入糖原。（摘要截断于250字）
