Abstract

The purpose of this study was to test the hypothesis that increased substrate (glucose) availability will enhance fatty acid synthesis in the growth retarded rat fetus. At 17 days of gestation, 19 time-dated pregnant rats had one uterine artery ligated, leading to growth retardation (IUGR) in the fetuses located on the uterine horn supplied by the ligated artery. The uterine artery of the opposite uterine horn was left untouched, resulting in appropriately grown fetuses, which served as controls. At 21 days of gestation the animals were infused with either 20% dextrose or 0.9% saline via a maternal jugular vein catheter for 4 hr. Fetal organ fatty acid synthesis was measured by maternal 3H 2O injection. In the growth retarded saline infused fetus, specific activity for 3H (representing rate of fatty acid synthesis) was significantly lower in fetal liver, lung and carcass. Dextrose infusion resulted in increased fatty acid synthesis in both control and IUGR fetuses in all tissues cited above. The specific activity in glucose infused IUGR fetal organs equalled that of saline infused control fetuses. The data indicate that maternal glucose infusion resulted in an increased rate of fatty acid synthesis, in IUGR fetuses; consequently, the deficit in fatty acid synthesis in the IUGR fetus (compared to appropriately grown control fetuses) was abolished.

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