Glucocorticoids regulate the ontogenetic transition of adrenergic receptor subtypes in rat liver.

摘要: Abstract During neonatal development, adrenergic control of hepatic glucose metabolism undergoes a transition from β-receptor to α 1 -receptor-mediated dominance, coincident with the onset function hypothalamus-pituitary-adrenocortical axis at conclusion third fourth week postpartum. To determine whether glucocorticoids contribute this switch, rats were given mg/kg dexamethasone on postnatal days 13, 14 and 15 receptor population examined by radioligand binding techniques. Dexamethasone accelerated maturational replacement β-receptors -subtype; loss was not reversible upon discontinuing treatment. When glucocorticoid earlier, 7, 8 9, similar effects obtained, but suppression β-subtype only temporary; treatment before parturition (gestational 17, 18 19) failed suppress binding. These results suggest that, during critical period, adrenocorticosteroids provide important signal for function.