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Baudrie V, Chaouloff F. 
“Mechanisms involved in the hyperglycemic effect of the 5-HT1C/5-HT2 receptor agonist, DOI”. 
Eur J Pharmacol. 1992 Mar 14;213(1):41-6.
Previous experiments have indicated that 5-HT2 receptors and catecholaminergic systems mediate the rise in plasma glucose levels elicited by acute administration of the 5-HT1c/5-HT2 receptor agonist, 1-2,5-dimethoxy-4-iodophenyl-2-aminopropane DOI. On this basis, we investigated the location of these serotonin receptors and the nature of this catecholaminergic involvement. Administration of DOI 0.4 mg/kg i.v. to conscious rats bearing jugular catheters elicited a rapid rise in plasma glucose which was associated with a decreased insulin response to a glucose bolus 300 mg/kg i.v.. Pretreatment with the peripherally acting 5-HT1c/5-HT2 receptor antagonist, BW 501C67 0.5 mg/kg i.v. 10 min beforehand prevented the rise in plasma glucose triggered by the peripherally acting 5-HT1c/5-HT2 receptor agonist, alpha-methyl-5-HT 0.75 mg/kg i.v., but amplified the rise elicited by DOI. Pretreatment with chlorisondamine 1 mg/kg i.v. 10 min beforehand or adrenalectomy 20 h beforehand prevented the DOI-induced hyperglycemia. On the other hand, pretreatment with dexamethasone 0.35 mg/kg s.c. 2 h and 20 min beforehand did not affect the DOI-induced hyperglycemia. It is concluded that the hyperglycemic effect of DOI administration is mediated by centrally located 5-HT2 receptors and, in turn, adrenal epinephrine release.
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