Chronic maternal ethanol administration in the rat decreases the stimulation by (-) epinephrine of glycogen phosphorylase a in the livers of the progeny during development.

Abstract

Previous results from this laboratory have shown that the progeny of alcoholic rats have diminished alpha 1-adrenergic receptors in the hepatic plasma membranes. Since these receptors mediate epinephrine action on glycogen metabolism, it was decided to determine whether this change might affect the activation of glycogen phosphorylase a in the livers of the alcoholic progeny. Pregnant female rats were divided into two groups of which one received a Metrecal-ethanol liquid diet throughout pregnancy and lactation. The pair-fed control group received a liquid sucrose-Metrecal diet over the same period. Phosphorylase a activity was determined in liver slices from the progeny during postnatal development. The basal hepatic phosphorylase a activity was identical between the control and experimental groups at 5, 15 and 25 days of age. Both epinephrine and phenylephrine were superior enzyme activators than was isoproterenol. Stimulation with epinephrine (10 microM) demonstrated a significantly diminished capacity of the enzyme in the alcoholic liver to be activated by the hormone. In every instance, the livers from 5, 15 and 25 day old pups from alcoholic mothers displayed diminished epinephrine-stimulated phosphorylase a activity of about 30%, compared with the controls.