Citation

Sakata T, Kang M, Kurokawa M, Yoshimatsu H. Obes. Res. 1995; 3 Suppl 5: 707S-712S.

Copyright

(Copyright © 1995, North American Association for the Study of Obesity)

DOI

10.1002/j.1550-8528.1995.tb00489.x

PMID

8653552

Abstract

Homeostatic involvement of hypothalamic neuronal histamine in adaptive behavior and thermogenesis was investigated when interleukin-1 beta (IL-1 beta), one of the endogenous pyrogens, was infused peripherally in rats. IL-1 beta decreased food and water intake and elevated body temperature. Depletion of neuronal histamine in the hypothalamus induced by alpha-fluoromethylhistidine, a suicide inhibitor of the histamine synthesizing enzyme histidine decarboxylase (HDC), attenuated the suppressive effect of IL-1 beta on food intake, facilitated the inhibitory effect on water intake, and enhanced its thermogenic effect. Simultaneously IL-1 beta increased activity of HDC and histamine-N-methyltransferase (HMT), a neuronal histamine catabolizing enzyme. Pretreatment with indomethacin completely blocked those increases in turnover of neuronal histamine induced by IL-1 beta. Hypothalamic prostaglandin E2 (PGE2) activated by peripheral IL-1 beta, but not peripheral PGE2, increased both activities of HDC and HMT. Ginsenoside Rg1, a major component of panax ginseng, modulated the suppressive effects of IL-1 beta on ingestive behavior, resulting in a lowering of body temperature. The findings suggest that the effects of IL-1 beta on ingestive behavior and thermogenesis may be modulated by dynamics of hypothalamic neuronal histamine through activation of hypothalamic PGE2 which is elevated by peripheral IL-1 beta.

Language: en

Keywords

Adaptation, Physiological; Animals; Body Temperature Regulation; Central Nervous System Agents; Dinoprostone; Drugs, Chinese Herbal; Eating; Ginsenosides; Histamine; Hypothalamus; Interleukin-1; Neurons; Rats; Saponins