Placental Transfer of Analogs of Glucose and Amino Acids in Experimental Intrauterine Growth Retardation

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Abstract

Summary

We have employed the model in which one uterine artery is ligated to study maternofetal transport and tissue uptake of glucose and amino acids in the intrauterine growth-retarded rat. On the 18th day of gestation, the artery supplying one uterine horn was ligated. Two days later the rats received [3H]2-deoxyglucose and |14C]α-aminoisobutyric acid iv. One hour later the growth-retarded and control fetuses were delivered by Cesarean section and appropriate blood samples were obtained. The growth-retarded fetuses had an average weight reduction of 27%, significantly increased placental to fetal weight ratio and brain to body ratio, and a significantly reduced liver to body ratio. Total radioactivity derived from tritiated deoxyglucose in whole fetal tissues, placenta, liver, and brain were significantly decreased in the intrauterine growth-retarded (IUGR) fetuses; this was also true per gram of tissue except for liver. Liver to plasma, brain to plasma, and whole fetal tissue to plasma 3H ratios were significantly increased in the IUGR group. The radioactivity derived from [14C]α-aminoisobutyric acid was significantly reduced in whole fetal tissues, placenta, liver, and brain in the IUGR fetuses whether expressed per whole organ or per gram of tissue. Significant differences in liver to plasma, brain to plasma, and whole tissue to plasma 14C ratios were not observed.

Speculation

The large reduction in maternofetal transfer of deoxyglucose and α-aminoisobutryric acid when uterine blood flow is reduced raises the possibility that one of the major causes of retarded growth in utero is a diminished supply of glucose and amino acids to the fetus. The fetal liver appears to be especially effective in increasing its extraction of 2-deoxyglucose from fetal plasma during this period of nutrient restriction. Since a major cause of fetal growth retardation in man is an impairment in maternal circulatory supply to the placenta, a similar mechanism of growth retardation may contribute to human IUGR. The possibility that nutritional supplementation may be of value in improving the growth conditions for the fetus when uterine blood flow is restricted would seem worthy of further investigation. More information is also required about the mechanisms responsible for the apparent improved extraction of glucose from plasma in IUGR.

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