Pollak A, Susa J B, Stonestreet B S, Schwartz R, Oh W
Pediatr Res. 1979 Mar;13(3):175-7. doi: 10.1203/00006450-197903000-00008.
This study examines the role of impaired gluconeogenesis in the pathogenesis of neonatal hypoglycemia in intrauterine growth retardation (IUGR). IUGR was produced experimentally in eight pregnant rats by ligation of uterine arteries at the 17th day of gestation. Delivery occurred spontaneously at term. Sham operations were performed in five pregnant rats at the same gestational age and the fetuses delivered at term served as controls. The body weights of newborn rats with IUGR were significantly lower than the controls (5.32 +/- 0.12 vs. 6.22 +/- 0.06 g, mean +/- SE, P less than 0.001). The fetal liver weights were also significantly smaller in IUGR than in the control animals (0.224 +/- 0.14 vs. 0.340 +/- 0.12 g, P less than 0.001). The activity of phosphoenolpyruvate carboxykinase (PEPCK) (the rate-limiting enzyme of gluconeogenesis) in liver cytosols was significantly lower in rats with IUGR (0.06 +/- 0.01 vs. 0.11 +/- 0.02 microM phosphoenolpyruvate/g liver/min when compared with controls (P less than 0.05). A direct relationship between this enzyme and the birth weight was observed, suggesting a close relationship between intrauterine nutrition and the status of gluconeogenesis. The blood glucose level was also lower in growth-retarted fetuses (36.6 +/- 4.7 vs. 69.6 +/- 4.3 mg/dl, p less than 0.001) when compared with controls. The data suggest that gluconeogenesis is impaired in IUGR and is partly responsible for the increase in the incidence of neonatal hypoglycemia in this group of subjects.
