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Glucose homeostasis in the newborn

Robert Hume1, Ann Burchell, Fiona L R Williams

  • 1Maternal and Child Health Sciences, University of Dundee, Ninewells Hospital and Medical School, Dundee DD1 9SY Scotland, UK. r.hume@dundee.ac.uk

Early Human Development
|February 15, 2005
PubMed

Insights

Preterm infants often experience blood sugar regulation issues due to delayed enzyme development. This can lead to hypoglycemia or hyperglycemia, impacting their overall glucose homeostasis.

Area of Science:

  • Biochemistry
  • Pediatrics
  • Endocrinology

Background:

  • Hepatic glucose production, via glycogenolysis and gluconeogenesis, is vital for maintaining blood glucose levels.
  • The glucose-6-phosphatase system is critical for both pathways, but its postnatal upregulation is often delayed in preterm infants.
  • Failures in glucose homeostasis regulation are observed in specific groups of preterm infants.

Purpose of the Study:

  • To investigate the mechanisms behind glucose homeostasis dysregulation in preterm infants.
  • To identify clinical and hormonal characteristics of preterm infants at risk of hypoglycemia or hyperglycemia.
  • To explore the role of hormonal dysfunctions in the postnatal expression of hepatic enzymes.

Main Methods:

  • Observational study comparing preterm infants with and without glucose homeostasis issues.
  • Measurement of hormonal levels (cortisol, corticotrophin, epinephrine, insulin, glucagon, human growth hormone).
  • Assessment of glycaemic response to glucagon and insulin sensitivity.

Main Results:

  • Up to 20% of preterm infants at discharge risk hypoglycemia with delayed feeding; these infants show elevated cortisol, corticotrophin, and epinephrine.
  • 30% of preterm infants at discharge exhibit inadequate glycaemic response to glucagon, presenting with relative fasting hyperglycemia, hyperinsulinaemia, and altered insulin:glucagon ratios.
  • No significant differences in insulin, glucagon, or human growth hormone levels were found between hypoglycemic and normoglycemic infants.

Conclusions:

  • Developmental delays in hepatic glucose-6-phosphatase enzyme activity contribute to glucose dysregulation in preterm infants.
  • Preterm infants can present with distinct patterns of glucose homeostasis failure, including hypoglycemia and hyperglycemia.
  • Hormonal dysfunctions may play a role in the impaired postnatal expression of hepatic enzymes essential for glucose metabolism.

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