title: Fetal-perinatal catecholamine secretion: role in perinatal glucose homeostasis.
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.
mesh_terms: D000818:Animals; D004837:Epinephrine / Q000378:metabolism* / Q000494:pharmacology; D005260:Female; D005333:Fetus / Q000187:drug effects / Q000378:metabolism*; D005934:Glucagon / Q000378:metabolism; D005943:Gluconeogenesis; D005947:Glucose / Q000378:metabolism*; D006706:Homeostasis; D006801:Humans; D007231:Infant, Newborn; D007328:Insulin / Q000378:metabolism; D008431:Maternal-Fetal Exchange; D009638:Norepinephrine / Q000378:metabolism* / Q000494:pharmacology; D011247:Pregnancy; D011972:Receptor, Insulin / Q000378:metabolism; D011941:Receptors, Adrenergic / Q000378:metabolism / Q000502:physiology; D011956:Receptors, Cell Surface / Q000378:metabolism; D018027:Receptors, Glucagon; D012756:Sheep / Q000196:embryology
chemical_list: D007328:Insulin; D011941:Receptors, Adrenergic; D011956:Receptors, Cell Surface; D018027:Receptors, Glucagon; D005934:Glucagon; D011972:Receptor, Insulin; D005947:Glucose; D009638:Norepinephrine; D004837:Epinephrine