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Fetal-perinatal catecholamine secretion: role in perinatal glucose homeostasis
Insights
Newborns experience significant hormonal shifts, including increased catecholamines (epinephrine and norepinephrine), to initiate vital metabolic processes like glucose production after birth. This transition is crucial for extrauterine survival.
Area of Science:
- Neonatal physiology
- Endocrinology
- Perinatal adaptation
Background:
- Catecholamine secretion is vital for neonatal adaptation, particularly for metabolic adjustments like glucose production.
- Fetal hypoxia significantly increases fetal plasma epinephrine and norepinephrine levels.
- Adrenergic receptor maturation occurs late in gestation, preparing for birth.
Purpose of the Study:
- To investigate the role of catecholamines in the transition from fetal to neonatal life.
- To understand the hormonal and metabolic changes occurring at birth.
- To explore the impact of catecholamine surge on glucose production and other metabolic pathways.
Main Methods:
- Analysis of plasma catecholamine levels (epinephrine and norepinephrine) in fetuses and newborns.
- Assessment of hormonal changes including glucagon, cortisol, growth hormone, and insulin.
- Measurement of glucose production, glycogenolysis, gluconeogenesis, lipolysis, and ketogenesis.
- Infusion studies of epinephrine and norepinephrine in fetal sheep.
Main Results:
- Plasma epinephrine and norepinephrine surge significantly at birth, with higher levels in hypoxic infants.
- Glucagon, cortisol, and growth hormone increase, while insulin remains low and unresponsive.
- Glucose production and gluconeogenesis, absent in utero, become active post-birth.
- Catecholamine infusion in fetal sheep mimicked the hormonal and metabolic profile of birth.
Conclusions:
- The spontaneous surge in catecholamines at birth is a key event triggering essential metabolic adaptations.
- These hormonal changes activate pathways necessary for survival outside the womb, such as endogenous glucose production.
- Understanding this transition is critical for managing neonatal metabolic health.
Abstract:
Secretion of catecholamines may play an important role in several of the adaptations that characterize the transition from intra- to extrauterine life including cardiovascular, respiratory, and metabolic events, specifically the initiation of endogenous glucose production following curtailment of the transplancental maternal supply of glucose. Maturation of neural and enzymatic pathways involved in catecholamine secretion occurs late in gestation; fetal hypoxia can produce a 20- and 125-fold increase in plasma epinephrine (E) and norepinephrine (NE), respectively. Estimates of turnover (approximately 2,000 pg X kg-1 X min-1) and metabolic clearance rates (20-40 ml X kg-1 X min-1) indicate active secretion and metabolism of E from fetal sources with negligible transfer from the mother. Simultaneously, there is maturation of functional alpha- and beta-adrenergic receptors. At birth, plasma E and NE rise three- to tenfold; plasma levels are higher in hypoxic infants and lower in prematures. Concurrently, glucagon increases three- to fivefold; cortisol and growth hormone also are high, whereas insulin remains low and poorly responsive to stimuli; the number of glucagon receptors increases, whereas that of insulin decreases. Acting in concert these hormonal changes activate glycogenolysis, gluconeogenesis, lypolysis, and ketogenesis. Glucose production and gluconeogenesis, absent in utero, become evident within hours of birth in both humans and sheep. The spontaneous surge in catecholamine secretion at birth may be the key event because infusion of E or NE to fetal sheep in late gestation simulates the metabolic and hormonal profile of glucagon and insulin as well as glucose production that normally only occur with separation of the placenta.