In vitro palmitate and glucose metabolism in the postmature fetus.
Fetuses from term and postmature rabbits were obtained and their livers incubated with palmitate-1-14C in room air. The net incorporation of the fatty acids into ketone bodies, lipids, and Co2 was measured at fixed and variable concentrations of cold glucose. Data from postmature liver show that lipid synthesis is decreased, 14CO2 production is increased, and ketone body formation is unchanged when compared with data from the term liver. The addition of cold glucose to a constant concentration of palmitate-1-14C causes a slight increase in lipid synthesis in thepostmature liver, in contrast to a decrease in the term liver. The experimental results indicate that liver lipid synthesis and glucose utilization are diminished in the postmature preparation. This suggests that the postmature fetal liver responds to the decreased availability of free fatty acid from the placenta and to the increasing hypoxia by metabolic adaptations resembling those observed during fasting and tissue hypoxia. These changes are somewhat similar to those observed in the neonate before the onset of breast-feeding. Fetal metabolism is, therefore, responsive to changes in placental transfer of fatty acids and to postmaturity.
D000818:Animals; D002245:Carbon Dioxide / Q000032:analysis; D005230:Fatty Acids, Nonesterified / Q000378:metabolism; D005260:Female; D005333:Fetus / Q000378:metabolism*; D005865:Gestational Age; D005947:Glucose / Q000378:metabolism*; D066298:In Vitro Techniques; D007657:Ketone Bodies / Q000032:analysis; D008055:Lipids / Q000096:biosynthesis; D008099:Liver / Q000378:metabolism*; D008431:Maternal-Fetal Exchange; D010168:Palmitates / Q000378:metabolism*; D010169:Palmitic Acids / Q000378:metabolism*; D010927:Placental Insufficiency / Q000378:metabolism; D011247:Pregnancy; D011817:Rabbits
D005230:Fatty Acids, Nonesterified; D007657:Ketone Bodies; D008055:Lipids; D010168:Palmitates; D010169:Palmitic Acids; D002245:Carbon Dioxide; D005947:Glucose