Abstract

Metoprine is a histamine N-methyltransferase inhibitor that elevates endogenous histamine (HA) levels. Because the histaminergic mechanism may be involved in the regulation of feeding behavior as well as in body glucose homeostasis, the effect of metoprine on glucoprivic feeding was studied in Wistar rats. Although metoprine treatment (10 and 20 mg/kg, IP) decreased feeding, the rats still responded to the administration of 400 mg/kg of 2-deoxy- D-glucose (2-DG) by increasing their feed intake. No difference was seen in the 6-h cumulative feed intake after administration of 2-DG between the metoprine- and solvent-treated rats. However, the response was delayed, and with 20 mg/kg metoprine the feed intake was significantly reduced during 2 h after 2-DG application. Both 2-DG and metoprine elevated plasma glucose concentration despite their opposite effects on feeding. Hypothalamic HA or its metabolite levels were not affected by 2-DG. The results suggest that the effects of metoprine and 2-DG are largely independent of each other, and that the feeding modulating function of HA is on such a level that it does not prevent the glucoprivic emergency response.

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