2-deoxy-D-glucose suppresses food intake through activation of hypothalamic histamine in rats.
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.
Sakata
T
T
Department of Internal Medicine I, School of Medicine, Oita Medical University, Japan.
Tamari
Y
Y
Kang
M
M
Yoshimatsu
H
H
D000818:Animals; D003847:Deoxyglucose / Q000494:pharmacology*; D004435:Eating / Q000187:drug effects*; D006632:Histamine / Q000378:metabolism*; D006633:Histamine Antagonists / Q000494:pharmacology; D007031:Hypothalamus / Q000378:metabolism*; D007274:Injections, Intraperitoneal; D007276:Injections, Intraventricular; D008297:Male; D008762:Methylhistidines / Q000494:pharmacology; D051381:Rats; D017208:Rats, Wistar
D006633:Histamine Antagonists; D008762:Methylhistidines; C028309:alpha-fluoromethylhistidine; D006632:Histamine; D003847:Deoxyglucose