Journal List > Korean J Perinatol > v.27(2) > 1013802

Cho and Chung: Glucose Homeostasis during Fetal and Neonatal Period

Abstract

Glucose is essential for energy metabolism in human, especially in brain, and is a source of energy storage in the form of glycogen, fat and protein. During fetal life, the predominant source of energy is also glucose, which crosses the placenta by facilitated diffusion. There is very little endogenous glucose production under normal circumstances during fetal life. During labor, the fetus is exposed to physiological challenges that require metabolic adaptation. A healthy infant successfully manages the postnatal transition by mobilizing and using alternative. After birth, there is a rapid surge in catecholamine and glucagon levels, and a steady decrease in insulin, as blood glucose levels decline. These hormonal changes induce enzyme activities that lead to glycogenolysis and gluconeogenesis. During the first 24-48 hours of life, plasma glucose concentrations of neonates are typically lower than later in life. Distinguishing between transitional neonatal glucose regulation in normal neonates and hypoglycemia that persists or occurs for the first time beyond the first 72 hours of life is important for prompt diagnosis and treatment to avoid serious consequences.

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Fig. 1
Screening for and management of postnatal glucose homeostasis in late-preterm (gestational age 34 –36+6 weeks) and term smallfor-gestational age infants and infants who were born to mothers with diabetes, large-for-gestational age infants. Modified from Pediatrics 2011;127:575-9.8
kjp-27-95f1.tif
Table 1.
Metabolic Transition from Fetus and Neonate
Metabolic function Fetus Neonate
Source of nutrients Mother Endogeneous
Endogenous glucose production Minimal Active
Lipolysis/Ketogenesis Minimal Active
Dominant metabolism Anabolism Catabolism
Hormone concentration    
  Insulin Low Low
  Glucagon Low High
  Epinephrine Low High
Hormone receptor    
  Insulin receptor density High Decrease
  Insulin receptor affinity High Decrease
  Glucagon receptor density Low Rapid increase
Enzyme concentration    
  Phosphorylase Low High
  PEPCK Low High

Abbreviation: PEPCK, phosphoenolpyruvate carboxykinase Adopted from Indian J Endocrinol Metab 2013;17:60-8.18

Table 2.
Neonates at Increased Risk for a Persistent Hypoglycemia Disorder
Neonates at increased risk of hypoglycemia and require glucose screening
1. Symptoms of hypoglycemia
2. Large for gestational age (even without maternal diabetes)
3. Perinatal stress
  a. Birth asphyxia/ischemia; cesarean delivery for fetal distress
  b. Maternal preeclampsia/eclampsia or hypertension
  c. Intrauterine growth restriction (small for gestational age)
  d. Meconium aspiration syndrome, erythroblastosis fetalis, polycythemia, hypothermia
4. Premature or postmature delivery
5. Infant of diabetic mother
6. Family history of a genetic form of hypoglycemia
7. Congenital syndromes (eg, Beckwith-Wiedemann), abnormal physical features (eg, midline facial malformations, microphallus)
Neonates in whom to exclude persistent hypoglycemia before discharge
1. Severe hypoglycemia (eg, episode of symptomatic hypoglycemia or need for IV dextrose to treat hypoglycemia)
2. Inability to consistently maintain preprandial PG concentration >50 mg/dL up to 48 hours of age and >60 mg/dL after 48 hours of age
3. Family history of a genetic form of hypoglycemia
4. Congenital syndromes (eg, Beckwith-Wiedemann), abnormal physical features (eg, midline facial malformations, microphallus)

Adopted from J Pediatr 2015;167:238-45.5

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