Endocrinology, Vol 130, 1325-1330, Copyright © 1992 by Endocrine Society
Beta-endorphin inhibits hypoglycemia-induced gene expression of corticotropin-releasing factor in the rat hypothalamus
T Suda, Y Sato, T Sumitomo, Y Nakano, F Tozawa, I Iwai, M Yamada and H Demura
Department of Medicine, Tokyo Women's Medical College, Japan.
Endogenous opioid peptides have a role in the regulation of the
hypothalamic-pituitary-adrenal axis. Recently, beta-endorphin (EP) has been
thought to inhibit CRF release in vivo and in vitro. In the present study
we examined the effects of central administration of EP on ACTH secretion
and gene expression of both CRF in the hypothalamus and POMC in the
anterior pituitary gland (AP) during basal and insulin- induced
hypoglycemia in pentobarbital-anesthetized rats. Administration of EP in
the lateral ventricle decreased basal CRF levels in the median eminence and
inhibited basal and hypoglycemia-induced ACTH secretion in a dose-dependent
manner. Hypoglycemia-induced POMC mRNA levels in the AP and CRF mRNA levels
in the hypothalamus were also dose-dependently inhibited by the
administration of EP. The inhibitory effect of EP was reversed by naloxone.
These results suggest that 1) central administration of EP acts through the
opioid receptor to inhibit hypoglycemia-induced CRF gene expression in the
hypothalamus and CRF release, which results in a decrease in ACTH secretion
and POMC mRNA levels in the AP; and 2) the active site of EP is the CRF
neuron in the paraventricular nucleus.
