Citation

Sakata T, Tamari Y, Kang M, Yoshimatsu H. Am. J. Physiol. 1994; 267(2 Pt 2): R616-618.

Copyright

(Copyright © 1994, American Physiological Society)

DOI

10.1152/ajpregu.1994.267.2.R616

PMID

8067475

Abstract

The aim of this experiment was to demonstrate whether brain histamine contributes to delayed suppression of food intake after administration of 2-deoxy-D-glucose (2-DG). Food intake decreased significantly for 48 h after infusion of 2-DG into the rat third cerebroventricle. This delayed decrease in food intake was abolished by depletion of neuronal histamine by intraperitoneal pretreatment with alpha-fluoromethylhistidine (160 mumol/rat), a suicide inhibitor of a histamine-synthesizing enzyme. Intracerebroventricular infusion of 24 mumol 2-DG accelerated turnover rate of hypothalamic histamine. These results indicate that the delayed feeding suppression by 2-DG is modulated through histaminergic neurons in the hypothalamus. This histaminergic response may be related, at least in part, to homeostatic control of energy metabolism in the brain.

Language: en

Keywords

Animals; Deoxyglucose; Eating; Histamine; Histamine Antagonists; Hypothalamus; Injections, Intraperitoneal; Injections, Intraventricular; Male; Methylhistidines; Rats; Rats, Wistar