FETAL GLUCOSE-METABOLISM AND OXYGEN-CONSUMPTION DURING SUSTAINED HYPOGLYCEMIA
FETAL GLUCOSE-METABOLISM AND OXYGEN-CONSUMPTION DURING SUSTAINED HYPOGLYCEMIA
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DOI：
10.1016/0026-0495(90)90075-n
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发表时间：
1990-02-01
影响因子：
9.8
通讯作者：
HAY, WW
中科院分区：
文献类型：
--
作者：
DIGIACOMO, JE;HAY, WW
本研究旨在探讨母体慢性高胰岛素血症和低血糖对胎儿糖代谢和胎儿生长的影响。在慢性母体胰岛素输注诱导的中度（第2组，n = 6）或显著（第3组，n = 6）母体低血糖期间，在长期插管的妊娠晚期胎羊中测量脐葡萄糖摄取（UGU）、胎仔葡萄糖利用率（GUR）、氧化分数（GOxF）和胎仔内源性葡萄糖产生率（EGPR）。 与血糖正常对照组（第1组，n = 10）相比，第2组中度低血糖动物的母体葡萄糖浓度（GA）降低38.5%，随后胎儿葡萄糖浓度（Ga）降低40.3%，胎儿胰岛素浓度（Ia）降低64%，UGU降低28.9%。第2组胎儿GUR下降13.1%。在第1组动物中未发现显著的EGPR;由于数值范围较宽，第2组的可测量EGPR与零无统计学差异。在第3组明显低血糖动物中，GA比对照组低57.4%，Ga、Ia和UGU分别降低45.9%、64%和75.7%。然而，GUR仅下降了19.6%，这是由于出现了显著的胎儿EGPR 2.81 ±。0.32 mg/min/kg。第2组和第3组动物的胎仔GUR均高于预测范围（平均值± 0.0001）。1 SEM）与我们的胎儿GUR对葡萄糖和胰岛素浓度变化的反应模型进行比较。在相同胎龄时，第2组和第3组尸检时的胎儿体重低于第1组对照组（P <0.05）。我们的结论是，胎儿葡萄糖可用性降低导致胎儿低血糖和低胰岛素血症，胎儿内源性葡萄糖产生的发展，胎儿生长迟缓。
The present study was conducted to determine the effects of chronic maternal hyperinsulinemia and hypoglycemia on fetal glucose metabolism and fetal growth. Umbilical glucose uptake (UGU), fetal glucose use rate (GUR), and oxidation fraction (GOxF), and fetal endogenous glucose production rate (EGPR) were measured in chronically catheterized, late gestation fetal lambs during moderate (group 2, n = 6) or marked (group 3, n = 6) maternal hypoglycemia induced by chronic maternal insulin infusion. Compared with normoglycemic controls (group 1, n = 10), group 2 moderate hypoglycemic animals had a 38.5% reduction in maternal glucose concentration (GA) with a subsequent 40.3% fall in fetal glucose concentration (Ga), 64% decrease in fetal insulin concentration (Ia), and a 28.9% decrease in UGU. Group 2 fetal GUR fell 13.1%. No significant EGPR was found in group 1 animals; group 2 had a measurable EGPR that was not statistically different from zero due to the wide range of values. In group 3 marked hypoglycemic animals GA was 57.4% lower than controls, and Ga, Ia, and UGU were reduced 45.9%, 64%, and 75.7%, respectively. However, GUR fell by only 19.6% due to the appearance of significant fetal EGPR of 2.81 .+-. 0.32 mg/min/kg. Fetal GUR in both group 2 and 3 animals were higher than the predicted range (mean .+-. 1 SEM) compared with our model of fetal GUR response to changes in glucose and insulin concentrations. Fetal weights at autopsy were lower in groups 2 and 3 than group 1 controls at the same gestational age (P < .05). We conclude that decreased fetal glucose availability leads to fetal hypoglycemia and hypoinsulinemia, development of fetal endogenous glucose production, and fetal growth retardation.