Sakata T, Kang M, Kurokawa M, Yoshimatsu H
Department of Internal Medicine I, School of Medicine, Oita Medical University, Japan.
Obes Res. 1995 Dec;3 Suppl 5:707S-712S. doi: 10.1002/j.1550-8528.1995.tb00489.x.
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.
当向大鼠外周注射内源性致热原之一的白细胞介素-1β（IL-1β）时，研究了下丘脑神经元组胺在适应性行为和产热中的稳态参与情况。IL-1β降低了食物和水的摄入量，并升高了体温。由组胺合成酶组氨酸脱羧酶（HDC）的自杀性抑制剂α-氟甲基组氨酸诱导的下丘脑神经元组胺耗竭，减弱了IL-1β对食物摄入的抑制作用，促进了对水摄入的抑制作用，并增强了其产热作用。同时，IL-1β增加了HDC和组胺-N-甲基转移酶（HMT，一种神经元组胺分解代谢酶）的活性。吲哚美辛预处理完全阻断了IL-1β诱导的神经元组胺周转率的增加。外周IL-1β激活的下丘脑前列腺素E2（PGE2），而非外周PGE2，增加了HDC和HMT的活性。人参的主要成分人参皂苷Rg1调节了IL-1β对摄食行为的抑制作用，导致体温降低。这些发现表明，IL-1β对摄食行为和产热的影响可能通过激活由外周IL-1β升高的下丘脑PGE2，由下丘脑神经元组胺的动态变化来调节。
