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Postmaturity in the rat: glucose metabolism in the fetus and the neonate
Insights
Postmature fetuses exhibit inhibited glucose synthesis and active glycogenolysis. Postmature newborns show delayed gluconeogenesis, leading to hypoglycemia unless fed, highlighting critical glucose metabolism differences.
Area of Science:
- Perinatal Medicine
- Neonatal Metabolism
- Endocrinology
Background:
- Postmature infants face unique metabolic challenges.
- Understanding glucose metabolism is crucial for neonatal care.
Purpose of the Study:
- Investigate glucose metabolism in postmature fetuses and newborns.
- Compare metabolic pathways between postmature and term neonates.
Main Methods:
- In vivo studies using [6-3H]glucose and [14C]lactate tracers.
- Measurement of hepatic glycogen content and radioactivity.
- Assay of phosphoenolpyruvate carboxykinase activity.
- Monitoring blood glucose and lactate levels postpartum.
Main Results:
- Fetal glycogenolysis is active, while synthesis is inhibited in prolonged gestation.
- Gluconeogenesis is inactive in fetuses and immediately postpartum in neonates.
- Postmature neonates show elevated gluconeogenesis by 3 hours postpartum.
- Fasting postmature neonates develop hypoglycemia by 6 hours postpartum due to weak gluconeogenesis.
- Fed postmature neonates maintain normal blood glucose via sustained gluconeogenesis.
Conclusions:
- Prolonged gestation alters fetal glucose metabolism, favoring glycogenolysis.
- Postmature neonates have a delayed but inducible gluconeogenic response.
- Nutritional support is critical for preventing hypoglycemia in postmature newborns.
Abstract:
The present study was designed to investigate glucose metabolism in the postmature fetus and newborn. In the fetus, the decreased hepatic glycogen content together with the decrease by the same percentage of total hepatic glycogen radioactivity from directly injected [6-3H]glucose demonstrate that fetal glycogenolysis occurs during prolonged gestation. Moreover, fetal glycogen synthesis as tested by in vivo [6-3H]glucose incorporation experiments is inhibited. In vivo experiments with [14C]lactate are consistent with gluconeogenesis, being inactive in the postmature fetus as well as in the normal-term fetus. During the first hr after delivery, our in vivo data about conversion of [14C]lactate to glucose show that the gluconeogenic pathway is not functioning in spite of very high phosphoenolpyruvate carboxykinase activity in the postmature. By 3 hr postpartum, the phosphoenolpyruvate carboxykinase activity, the blood lactate level, the percentage of conversion, and the rate of gluconeogenesis are very elevated in the postmatures as compared to the term neonates. By 6 hr postpartum, despite maintained phosphoenolpyruvate carboxykinase activity, gluconeogenic rate becomes very weak in postmatures kept fasting. This is the time characterized by a profound hypoglycemia. In contrast, fed postmature neonates exhibit normal blood glucose levels by 6 and 12 hr postpartum as a result of sustained rate of gluconeogenesis.