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Glucose production and oxidation in preterm infants during total parenteral nutrition
H N Lafeber1, E J Sulkers, T E Chapman
1Department of Pediatrics, Erasmus University Rotterdam, The Netherlands.
Insights
Preterm infants receiving total parenteral nutrition show suppressed endogenous glucose production. Glucose oxidation rates in these infants are approximately 63-65% of the infused glucose, with variations observed between appropriate and small for gestational age infants.
Area of Science:
- Neonatal Metabolism
- Pediatric Nutrition
- Endocrinology
Background:
- High glucose infusion rates during total parenteral nutrition (TPN) in preterm infants raise questions about endogenous glucose production suppression.
- Understanding glucose metabolism is crucial for optimizing nutritional support in vulnerable newborns.
Purpose of the Study:
- To investigate whether endogenous glucose production is fully suppressed in preterm infants receiving high rates of glucose via TPN.
- To compare glucose and carbohydrate oxidation rates in appropriate for gestational age (AGA) and small for gestational age (SGA) preterm infants.
Main Methods:
- Utilized a primed constant infusion of [U-13C] glucose in 1-week-old AGA and SGA preterm infants on TPN.
- Measured 13CO2 production in breath gas via isotope ratio mass spectrometry to determine glucose oxidation.
- Quantified plasma glucose production rates using gas chromatography mass spectrometry.
Main Results:
- Endogenous glucose production was negligible in both AGA and SGA preterm infants.
- Glucose oxidation rates were approximately 63-65% of the infused glucose in both groups.
- A significant difference between glucose and carbohydrate oxidation rates was observed in AGA infants, but not in SGA infants.
Conclusions:
- One-week-old AGA and SGA preterm infants on TPN exhibit no significant endogenous glucose production.
- Glucose oxidation accounts for 63-65% of infused glucose, suggesting efficient utilization.
- Observed metabolic differences between AGA and SGA infants may relate to lipogenesis or glycogen oxidation rates.
Abstract:
During total parenteral nutrition in preterm infants, glucose may be infused at high rates, but it is not known if the endogenous glucose production is fully suppressed under these circumstances. Eight preterm appropriate for gestational age (AGA) (birth wt: 1613 +/- 151 g, gestational age: 31.1 +/- 1.5 wk) and eight preterm small for gestational age (SGA) newborn infants (1185 +/- 241 g, 32.9 +/- 2.6 wk) receiving a glucose infusion rate of 7.55 +/- 0.56 and 8.16 +/- 0.65 mg/kg.min, respectively, were studied during continuous total parenteral nutrition at postnatal d 8. Glucose oxidation rate was determined with a primed constant infusion of [U-13C] glucose, measuring the 13CO2 production in breath gas by isotope ratio mass spectrometry and the glucose production rate in plasma by gas chromatography mass spectrometry. In breath gas of AGA and SGA infants, 60 and 65%, respectively, of the infused tracer appeared as 13CO2. The glucose production rates were 7.97 +/- 1.61 and 8.12 +/- 1.84 mg/kg.min in AGA and SGA infants, respectively, indicating that no significant endogenous glucose production occurred. The glucose oxidation calculated from the glucose production and 13CO2 production was 4.74 +/- 0.99 mg/kg.min in AGA infants and was significantly different from the carbohydrate oxidation rate of 6.62 +/- 1.23 mg/kg.min measured by simultaneous indirect calorimetry. In SGA infants, however, the glucose and carbohydrate oxidation rates were not significantly different at 5.33 +/- 1.56 and 6.16 +/- 2.45 mg/kg.min. It is concluded that 1-wk-old AGA or SGA preterm infants receiving total parenteral nutrition of 80 kcal/kg.d produce no endogenous glucose and their glucose oxidation rates are similar at 63-65% of the glucose infused. It is suggested that the significant difference between glucose and carbohydrate oxidation rates observed in AGA but not in SGA infants is due either to a higher rate of lipogenesis from carbohydrates, or, less likely, to a higher rate of glycogen oxidation.