Phosphoenolpyruvate Carboxykinase in Experimental Intrauterine Growth Retardation in Rats

Publisher Website
Google Scholar
Abstract
Summary: 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 < 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 < 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 μM phosphoenolpyruvate/g liver/min when compared with controls (P < 0.05). A direct relationship between this enzyme and the brith weight was observed, suggesting a close relationship between intrauterine nutrition and the status of gluconeogenesis. The blood glucose level was also lower in growth-retarded fetuses (36.6 ± 4.7 vs. 69.6 ± 4.3 mg/dl, p < 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. Speculation: Neonatal hypoglycemia in IUGR is probably caused by a combination of rapid depletion of glycogen stores and impaired gluconeogenesis, the latter indicated by a decreased liver PEPCK activity. This may be related to a diminished enzyme synthesis on the basis of significant energy and oxygen deprivation.

This publication has 3 references indexed in Scilit: