CNS beta-endorphin regulation of insulin-induced ornithine decarboxylase expression in liver of neonatal rats.
Previously, we reported that central (but not peripheral) administration of beta-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 beta-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 beta-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 beta-endorphin (1.5 mug/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 beta-endorphin was not reversed by naloxone, indicating that the effect is not mediated by brain mu or delta opioid receptors. Centrally administered beta-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 beta-endorphin may occur through actions on both basal ODC activity and tissue ODC sensitivity to "classical" trophic factors. The modulation by beta-endorphin of liver ODC expression apparently occurs distally to cAMP-generating mechanisms.
Bartolome
J V
JV
Department of Pharmacology, Duke University Medical Center, Durham, North Carolina 27710, USA.
Bartolome
M B
MB
Lorber
B A
BA
Schanberg
S M
SM