beta-Endorphin-induced hyperglycemia is mediated by increased central sympathetic outflow to adrenal medulla.
Synthetic human beta-endorphin increased plasma glucose concentration when administered intracisternally in chronically cannulated, conscious, unrestrained, adult male rats. This hyperglycemic effect of beta-endorphin was blocked by prior systemic administration of naloxone, supporting mediation of the effect at opioid receptors in brain. Adrenal denervation blocked the beta-endorphin-induced increase in plasma glucose, supporting a thesis that this effect is mediated at least in part by increased epinephrine secretion. The hyperglycemic response to intracerebral beta-endorphin was also blocked by either intracerebral hemicholinium-3 or somatostatin, supporting both a cholinergic link and a somatostatin neuron in the brain mechanism regulating endorphin-induced stimulation of sympathetic outflow.
D000313:Adrenal Medulla / Q000187:drug effects / Q000294:innervation*; D000818:Animals; D001786:Blood Glucose / Q000378:metabolism*; D003714:Denervation; D004723:Endorphins / Q000494:pharmacology*; D005260:Female; D006801:Humans; D006943:Hyperglycemia / Q000097:blood* / Q000139:chemically induced; D008297:Male; D009270:Naloxone / Q000494:pharmacology; D051381:Rats; D013564:Sympathetic Nervous System / Q000503:physiopathology*
D001786:Blood Glucose; D004723:Endorphins; D009270:Naloxone