GLUCOCORTICOIDS REGULATE THE ONTOGENIC TRANSITION OF ADRENERGIC-RECEPTOR SUBTYPES IN RAT-LIVER

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