Hypothalamic neuronal histamine modulates physiological responses induced by interleukin-1 beta

Kang, Masahiro; Yoshimatsu, Hironobu; Chiba, Seiichi; Kurokawa, Mamoru; Ogawa, Ryuichi; Tamari, Yuki; Tatsukawa, Mari; Sakata, Toshiie

doi:10.1152/ajpregu.1995.269.6.r1308

Cited by 20 publications

(21 citation statements)

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“…Indeed, histamine neuron activation suppresses food consumption in rats (34). Thermoregulation, a major factor involved in energy homeostasis, is mediated in part by brain histamine neurons (35). Energy deficiency in the brain, i.e., neural glucoprivation, activates histamine neurons in the hypothalamus (36) and augments glycogenolysis in the brain (37).…”

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confidence: 99%

Central Infusion of Histamine Reduces Fat Accumulation and Upregulates UCP Family in Leptin-Resistant Obese Mice

et al. 2001

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Leptin resistance has recently been confirmed not only in animal obese models but in human obesity. Evidence is rapidly emerging that suggests that activation of histamine signaling in the hypothalamus may have substantial anti-obesity and antidiabetic actions, particularly in leptin-resistant states. To address this issue, effects of central, chronic treatment with histamine on food intake, adiposity, and energy expenditure were examined using leptin-resistant obese and diabetic mice. Infusion of histamine (0.05 µmol · g body wt -1 · day -1 ) into the lateral cerebroventricle (i.c.v.) for 7 successive days reduced food intake and body weight significantly in both diet-induced obesity (DIO) and db/db mice. Histamine treatment reduced body fat weight, ob gene expression, and serum leptin concentration more in the model mice than in pair-fed controls. O besity, a common metabolic disorder characterized by chronic imbalance in energy intake and energy expenditure, is a serious risk factor for type 2 diabetes, coronary artery disease, hypertension, hyperlipidemia, and other common diseases (1). The pathophysiological basis of obesity, however, is poorly understood. Since discovery of the ob gene and its encoded protein leptin (2), it has been understood that leptin acts as a hormone at the level of the hypothalamus to inhibit food intake and favor energy expenditure (3-5). The uncoupling protein (UCP) family, consisting of inner mitochondrial proteins (6-9), is known to contribute to improvement of energy imbalance resulting from energy insufficiency or excess (7,10). Gene expression of the UCP family is highly responsive to neural and humoral factors (10-14), particularly leptin (14). Serum leptin thus reflects energy stores in adipose tissue and serves to signal the brain (15). To improve understanding of the leptin signaling pathway, a number of approaches have been tried to clarify the roles of leptin-modulated hypothalamic neuropeptides in the regulation of feeding behavior and energy homeostasis (16-18).Leptin negatively regulates orexigenic neuropeptide Y (16) and agouti gene-related protein (17) and positively regulates anorexigenic proopio-melanocortin-derived peptide through leptin receptors on neurons in the hypothalamic arcuate nucleus (18). Anorexigenic corticotropin-releasing hormone in the paraventricular nucleus, which negatively affects neuropeptide Y neurons in the arcuate nucleus (19), is also positively regulated by leptin (20). The signals from such sites in the mediobasal hypothalamus thus communicate the neural underpinning of hunger and satiety with the orexigenic mediators orexin (21) and melanocortin concentrating hormone (22), both of which originate in the lateral hypothalamus.Serum concentration of leptin is known to be increased in the great majority of obese humans as well as in most rodent models, indicating that most obesity is leptin resistant (23,24). Although the details and molecular basis of the mechanisms are unknown, important factors are indicated by the following findings. F...

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Central Infusion of Histamine Reduces Fat Accumulation and Upregulates UCP Family in Leptin-Resistant Obese Mice

et al. 2001

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“…In Figures 1, 2 and 3, FMH at a dose of 160 p o l h a t was pretreated into the peritoneum 1 hour before injection of 0.12 nmol/rat IL-lp into the peritoneum. As shown in those figures (16), FMH per se had no effect on inges- tive behavior or body temperature (16). When Fh4H was pretreated intraperitoneally, the feeding suppression induced by IL-lp was attenuated ( Figure 1).…”

Section: Hypothalamic Neuronal Histamine Modulates Ingestive Behaviormentioning

confidence: 71%

Hypothalamic Neuronal Histamine Modulates Adaptive Behavior and Thermogenesis in Response to Endogenous Pyrogen

et al. 1995

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Homeostatic involvement of hypothalamic neuronal histamine in adaptive behavior and thermogenesis was investigated when interleukin-lp (IL-lp), one of the endogenous pyrogens, was infused peripherally in rats. IL-1p decreased food and water intake and elevated body temperature. Depletion of neuronal histamine in the hypothalamus induced by a-fluoromethylhistidine, a suicide inhibitor of the histamine synthesizing enzyme histidine decarboxylase (HDC), attenuated the suppressive effect of IL-lp on food intake, facilitated the inhibitory effect on water intake, a n d enhanced its thermogenic effect. Simultaneously IL-lP 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-1p. Hypothalamic prostaglandin E2 (PGEi) activated by peripheral IL-lp, b u t not p e r i p h e r a l PGE2 , increased both activities of HDC a n d HMT. Ginsenoside Rgl, a major component of panax ginseng, modulated the suppressive effects of IL-lp on ingestive behavior, resulting in a lowering of body temperature. The findings suggest that the effects of IL-lp on ingestive behavior and thermogenesis may be modulated by dynamics of hypothalamic neuronal 1995;3(S~ppl5):707S-712S. histamine through activation of hypothalamic PGE2 which is elevated by peripheral JL-lp.

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“…The abnormalities in obese Zucker rats involve dysfunction of histaminergic neurons in the hypothalamus. It has been reported that the depletion of neuronal histamines in the hypothalamus mimicked the abnormalities of obese Zucker rats [67,72], and grafting of fetal hypothalamus of lean Zucker littermates into obese rats resulted in the attenuation of almost all the abnormalities [73].…”

Section: Suppression Of Food Intake By Histidinementioning

confidence: 99%

Role of Marine Foods in Prevention of Obesity

Nakajima

2010

Handbook of Seafood Quality, Safety and Health Applications

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Hypothalamic neuronal histamine modulates physiological responses induced by interleukin-1 beta

Cited by 20 publications

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Central Infusion of Histamine Reduces Fat Accumulation and Upregulates UCP Family in Leptin-Resistant Obese Mice

Central Infusion of Histamine Reduces Fat Accumulation and Upregulates UCP Family in Leptin-Resistant Obese Mice

Hypothalamic Neuronal Histamine Modulates Adaptive Behavior and Thermogenesis in Response to Endogenous Pyrogen

Role of Marine Foods in Prevention of Obesity

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