CNS β-endorphin regulation of insulin-induced ornithine decarboxylase expression in liver of neonatal rats

Abstract

Previously, we reported that central (but not peripheral) administration of β-endorphin to rat pups decreases basal ornithine decarboxylase (ODC; a growth-associated enzyme) activity throughout the body. This finding is consistent with the view that CNS β-endorphin is an important regulator of postnatal development. Insulin is a hormone that markedly affects liver growth and evidence indicates that this occurs, in part, through its ability to regulate ODC expression. The current study examines the effects of intracisternal injection of β-endorphin on the response of liver ODC to subcutaneous administration of insulin. Insulin (20 IU/kg body wt), markedly increased liver ODC activity in 2-, 4-, 6-, 10-, 18-, and 30-day-old rats. Intracisternal injection of β-endorphin (1.5 μg/g brain wt) inhibited this response to insulin in 2-, 4-, 6-, 10-, and 18-day-old rats, but not in 30-day-old animals. This inhibition by β-endorphin was not reversed by naloxone, indicating that the effect is not mediated by brain μ or δ opioid receptors. Centrally administered β-endorphin also blocked the increases in liver ODC activity evoked by subcutaneous administration of cAMP. The results from these studies suggest that the postulated regulation of postnatal development by CNS β-endorphin may occur through actions on both basal ODC activity and tissue ODC sensitivity to “classical” trophic factors. The modulation by β-endorphin of liver ODC expression apparently occurs distally to cAMP-generating mechanisms