Characterization of blood glucose level regulation in mouse opioid withdrawal models.

The regulation of blood glucose level in intracerebroventricular (i.c.v.) administration with opioid alone or opioid withdrawal model was studied in ICR mice. In the first group, we found that i.c.v. administered morphine or beta-endorphin alone causes an elevation of blood glucose level. Blood glucose level induced by i.c.v. morphine or beta-endorphin began to increase within 30min and reached maximal level at 1h, decreasing to the basal level after 2h. In another group, we observed that intraperitoneal (i.p.) injection with naloxone (10mg/kg) post-treated 3h after either a single i.c.v. injection with morphine or beta-endorphin did not affect the increased blood glucose level in either group. In the next study, we observed that multiple (1 time/day for 3 days) i.c.v. injection with morphine alone significantly increased the blood glucose level. However, i.p. injection with naloxone post-treated 3h after the last i.c.v. injection with morphine caused a decrease of blood glucose level. We found that multiple (1 time/day for 3 days) i.c.v. injections with beta-endorphin did not affect the blood glucose level. Furthermore, i.p. injection with naloxone did not affect the blood glucose level in the mice injected with multiply beta-endorphin. Our results suggest that both morphine and beta-endorphin administered i.c.v. acutely increases the blood glucose level. However, blood glucose levels in the groups of multiply administered morphine alone, beta-endorphin alone, and naloxone-treated withdrawal model in multiply injected morphine and beta-endorphin appear to be differentially regulated. Copyright 2010. Published by Elsevier Ireland Ltd.