[Ontogenesis of glucose regulation in neonate and consequences in neonatal management]

Glucose homeostasis during fetal life depends entirely on continuous placental glucose transfer. Fetal endocrine milieu is characterized by high insulin which has mainly anabolic action. During third trimester, insulin promotes energetic stores as glycogen and fat deposition. At birth, constant maternal supply is interrupted and this is accompanied by a surge in glucagon and catecholamine levels and a decrease in insulin level. These hormonal changes induce hepatic glucose production provided by glycogenolysis during the first hours of life and then by gluconeogenesis. They also promote lipolysis which generates glycerol, a gluconeogenic substrate and free fatty acids. Free fatty acids provide gluconeogenesis activating factors and ketone bodies which represent alternative fuels for brain metabolism. Equilibrium between tissue consumption of glucose, hepatic glucose production and exogenous glucose supply maintains blood glucose level. If one of these mechanisms fails, hypoglycaemia may occur. Hypoglycaemia is predictable in three situations: depletion of energetic stores (prematurity and intra-uterine growth restriction), increase tissue energetic consumption and fetal hyperinsulinism. Blood glucose levels at which clinical interventions should be considered depend on operational thresholds. Therapeutic goal in case of hypoglycaemia is to increase blood glucose enhancing gluconeogenesis and providing continuous brain supply with glucose and ketone bodies. Paradoxically, many preterm infants less than 30 gestational weeks develop hyperglycaemia. There is evidence that processing of proinsulin in beta-cells is deficient and that preterm infants are partially resistant to insulin. Exogenous insulin infusion is efficient and may be used with caution.