Chronic maternal hypoxia retards fetal growth and increases glucose utilization of select fetal tissues in the rat

The development of intrauterine growth retardation (IUGR) is frequently associated with fetal hypoxia, hypoglycemia, and abnormal fetal glucose metabolism. To determine the effects of hypoxia (without concomitant hypoglycemia) on fetal glucose metabolism, we continuously exposed pregnant rats to 10% (10.1 kPa) ambient oxygen from day 15 through day 20 of gestation (term, 21.5 days) and used radiolabeled 2-deoxyglucose (2DG) to measure in vivo relative glucose utilization (rGU) of several fetal tissues on day 20 of gestation. Pair-fed rats in room-air oxygen were used as controls. Maternal hypoxia resulted in significant IUGR, fetal hypoxia and acidosis, and fetal lactate accumulation on day 20 of gestation. Following 5 days of hypoxia, rGU values for fetal lung, heart, and kidney were increased by 61%, 54%, and 47%, respectively (P < .05). rGU values for fetal brain, liver, muscle, and placenta were not significantly affected. Fetal plasma glucose concentrations were similar in hypoxic and control fetuses. We speculate that the increased rGU of hypoxic fetal tissues is due in part to anaerobic metabolism and increased glycolysis.