Glucose homeostasis in the newborn

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.