Role of endorphins in endotoxin-induced hyperglycaemia in mice.
The present study assessed the role of endogenous opiate systems in the hyperglycaemic response to challenge with endotoxin in mice. Blockade of opiate receptors by administration of the opiate antagonists naloxone (1.0 mg/kg) or naltrexone (1.0 or 5.0 mg/kg) significantly decreased the degree of hyperglycaemia caused by challenge with endotoxin (80 micrograms). Naltrexone methyl bromide, a peripherally acting opiate antagonist, had no demonstrable effect on the endotoxin-induced hyperglycaemia. Finally, induction of tolerance to morphine prevented the hyperglycaemic response to challenge with endotoxin. These results suggest a causative role for central endorphinergic mechanisms in the hyperglycaemic response to administration of endotoxin. They support the view that the centrally acting opiate antagonist, by blocking the brain opiate receptors, can influence metabolic adaptation to endotoxin-induced shock.
D000818:Animals; D001786:Blood Glucose / Q000378:metabolism; D004361:Drug Tolerance; D004723:Endorphins / Q000502:physiology*; D004731:Endotoxins / Q000494:pharmacology*; D006943:Hyperglycemia / Q000139:chemically induced / Q000503:physiopathology*; D008297:Male; D051379:Mice; D008809:Mice, Inbred C3H; D009020:Morphine / Q000494:pharmacology; D009270:Naloxone / Q000494:pharmacology; D009271:Naltrexone / Q000494:pharmacology
D001786:Blood Glucose; D004723:Endorphins; D004731:Endotoxins; D009270:Naloxone; D009271:Naltrexone; D009020:Morphine