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Glucose metabolism in a term infant with transient hyperinsulinism and high carbohydrate intake

J B van Goudoever1, E J Sulkers, S C Kalhan

  • 1Department of Paediatrics, Sophia Childrens Hospital, Rotterdam, The Netherlands.

European Journal of Pediatrics
|April 1, 1993
PubMed

Insights

Transient hyperinsulinaemia causes hypoglycemia in newborns via increased non-oxidative glucose disposal, not oxidation. Newborns show significant lipogenesis capacity when given high carbohydrate intake.

Area of Science:

  • Neonatal Medicine
  • Pediatric Endocrinology
  • Metabolic Research

Background:

  • Transient hyperinsulinaemia is a common cause of hypoglycemia in neonates.
  • Hypoglycemia can result from decreased glucose production or increased glucose uptake.
  • The specific pathways of increased glucose disposal in neonatal hyperinsulinemic hypoglycemia remain unclear.

Observation:

  • A term infant with transient hyperinsulinaemia and hypoglycemia received high glucose infusions.
  • Indirect calorimetry and glucose turnover studies were conducted on day 6 (high carbohydrate intake) and day 11 (normalized intake).
  • Carbohydrate intake was 13.6 mg/kg/min on day 6 and 7.8 mg/kg/min on day 11.

Findings:

  • Glucose oxidation was 28% higher on day 6 compared to day 11.
  • Non-oxidative glucose disposal was 257% higher on day 6 compared to day 11.
  • Hypoglycemia in hyperinsulinism is primarily due to increased non-oxidative glucose disposal, not increased glucose oxidation.

Implications:

  • Neonatal hypoglycemia due to transient hyperinsulinaemia is characterized by enhanced non-oxidative glucose metabolism.
  • Newborns possess a substantial capacity for lipogenesis when subjected to high carbohydrate loads.
  • Understanding glucose disposal pathways is crucial for managing neonatal hypoglycemia and metabolic adaptation.

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