Evidence of central influences on blood glucose level: malathion hyperglycemia.
To suppress the hyperglycemic effect of malathion in rats, a smaller amount of atropine was required when the drug was injected by intraventricular (i. vent.) than s.c. Pentobarbital, but not diazepam, blocked the hyperglycemic response. The results suggest that central accumulation of acetylcholine was the mediator of the response. Since hyperglycemia was not abolished by adrenalectomy and/or hypophysectomy, a hypothesis is presented to explain how central accumulation of acetylcholine might cause hyperglycemia.
D000109:Acetylcholine / Q000378:metabolism; D000315:Adrenalectomy; D000818:Animals; D001285:Atropine / Q000494:pharmacology; D001786:Blood Glucose / Q000378:metabolism*; D001921:Brain / Q000378:metabolism; D002802:Cholinesterases / Q000097:blood; D003864:Depression, Chemical; D003975:Diazepam / Q000494:pharmacology; D005260:Female; D006943:Hyperglycemia / Q000139:chemically induced; D007016:Hypophysectomy; D008294:Malathion / Q000494:pharmacology*; D010424:Pentobarbital / Q000494:pharmacology; D051381:Rats; D014221:Triamcinolone / Q000494:pharmacology
D001786:Blood Glucose; D014221:Triamcinolone; D001285:Atropine; D002802:Cholinesterases; D010424:Pentobarbital; D000109:Acetylcholine; D003975:Diazepam; D008294:Malathion