title: Autonomic and endocrine participation in opioid peptide-induced hyperglycemia.
abstract: Intracisternal administration of synthetic human beta-endorphin to conscious, ambulatory adult male rats caused dose-related increases in plasma glucose concentration. The largest dose of beta-endorphin examined, 7.25 nmol, increased plasma glucose concentration within 7 min and this effect lasted 2.5 h. On the other hand, only 58 pmol was required to induce transient hyperglycemia, when compared to the response observed in saline-injected control rats. This hyperglycemic effect of beta-endorphin was prevented by prior systemic administration of naloxone, thus supporting the hypothesis that this beta-endorphin-induced effect is mediated at opioid receptors. beta-Endorphin also markedly increased plasma concentrations of epinephrine, norepinephrine and, to a lesser extent, dopamine. A significant positive correlation was demonstrated between plasma glucose and plasma epinephrine responses to increasing doses of intracisternally administered beta-endorphin. In addition, intracisternal beta-endorphin also increased plasma glucagon concentration without significantly increasing plasma insulin concentration. Thus, it is probable that epinephrine and glucagon are the major factors mediating this hyperglycemic effect. beta-Endorphin-induced hyperglycemia was prevented by ganglionic blockade with chlorisondamine. This further supports the thesis that intracerebral beta-endorphin increases plasma glucose concentration by activation of the central autonomic outflow. In addition to these effects on short-term regulators of glycemia, intracisternal beta-endorphin increased plasma concentrations of corticosterone and growth hormone. Both of these glucose counterregulatory hormones may play minor roles in modulating beta-endorphin-induced hyperglycemia.
authors.affiliation: Veterans Administration Medical Center, Lexington, KY 40511.
authors.forename: N M
authors.initials: NM
authors.lastname: Appel
authors.forename: N S
authors.initials: NS
authors.lastname: Track
authors.forename: G R
authors.initials: GR
authors.lastname: Van Loon
mesh_terms: D000324:Adrenocorticotropic Hormone / Q000097:blood; D000818:Animals; D002946:Cisterna Magna; D003345:Corticosterone / Q000097:blood; D004298:Dopamine / Q000097:blood; D004837:Epinephrine / Q000097:blood; D005934:Glucagon / Q000097:blood; D013006:Growth Hormone / Q000097:blood; D006943:Hyperglycemia / Q000139:chemically induced*; D007269:Injections, Intra-Arterial; D007276:Injections, Intraventricular; D007328:Insulin / Q000097:blood; D008297:Male; D009638:Norepinephrine / Q000097:blood; D051381:Rats; D011919:Rats, Inbred Strains; D011957:Receptors, Opioid / Q000502:physiology*; D001615:beta-Endorphin / Q000008:administration & dosage / Q000494:pharmacology*
chemical_list: D007328:Insulin; D011957:Receptors, Opioid; D001615:beta-Endorphin; D000324:Adrenocorticotropic Hormone; D013006:Growth Hormone; D005934:Glucagon; D004298:Dopamine; D003345:Corticosterone; D009638:Norepinephrine; D004837:Epinephrine