Blockade of the histamine H1-receptor in the rat ventromedial hypothalamus and feeding elicitation

Sakata, Toshiie; Ookuma, Kazuyoshi; Fukagawa, Koji; Fujimoto, Kazuma; Yoshimatsu, Hironobu; Shiraishi, Takeshi; Wada, Hiroshi

doi:10.1016/0006-8993(88)91423-0

Cited by 130 publications

(88 citation statements)

References 12 publications

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“…The released histamine controls ingestive behavior through histamine H1 receptors, which belong to a family of G protein (guanine nucleotide-binding regulatory proteins) coupled receptors (3,19,20), and induces anti-obesity effects such as feeding suppression, lipolysis in white adipose tissue (intracerebroventricular injection of histamine promotes glycerol release from white adipose tissue), and weight reduction (2-4). Moreover, histaminergic neurons are known to participate in regulating heat production (thermoregulation) and energy consumption.…”

Section: Discussionmentioning

confidence: 99%

Proline Decreases the Suppressive Effect of Histidine on Food Intake and Fat Accumulation

Asahi

Tanaka

Fujimi

et al. 2016

J Nutr Sci Vitaminol

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SummaryWe recently suggested that proline might decrease the suppressive effect of histidine on food intake. Our purpose in the present study was to investigate the influence of proline on the suppressive effect of histidine on food intake and accumulation of body fat. Male Wistar rats were divided into four groups and allowed free access to the following diets for 3 wk: control (C), 5% proline (P), 5% histidine (H), or 5% histidine plus 10% proline (HP) diets. Food intake for 7 d and retroperitoneal fat tissue weight at the end of the experimental period of the HP diet group were greater than those of the H diet group, whereas no significant difference existed between the HP diet group and the C diet group. Our results indicate that proline inhibits the influence of histidine on food intake and accumulation of body fat.

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Section: Discussionmentioning

confidence: 99%

Proline Decreases the Suppressive Effect of Histidine on Food Intake and Fat Accumulation

Asahi

Tanaka

Fujimi

et al. 2016

J Nutr Sci Vitaminol

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“…Brain histamine appears to suppress food intake via histamine H1 receptors. Centrally administered histamine H1 receptor agonists suppressed food consumption in rats (Lecklin et al, 1998), whereas injection of H1-antagonists elicited food intake (Sakata et al, 1988;Ookuma et al, 1993). However, relatively few studies have been carried out to unequivocally establish a relationship between food consumption and H1 receptors blockade in humans (Deng et al, 2010).…”

Section: Discussionmentioning

confidence: 99%

Pleiotropic effect of histamine H4 receptor modulation in the central nervous system

2013

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a b s t r a c tThe histamine H4 receptor (H4R) is expressed primarily on cells involved in inflammation and immune responses. Recently, it has been reported the functional expression of H4R within neurons of the central nervous system, but their role has been poorly understood. The present study aimed to elucidate the physiopathological role of cerebral H4R in animal models by the intracerebroventricular administration of the H4R agonist VUF 8430 (20e40 mg per mouse). Selectivity of results was confirmed by the prevention of the effects produced by the H4R antagonist JNJ 10191584 (3e9 mg/kg p.o.). Neuronal H4R activation induced acute thermal antinociception, indicating that neuronal histamine H4R might be involved in the production of antinociception in the absence of an inflammatory process. An anxiolyticlike effect of intensity comparable to that exerted by diazepam, used as reference drug, was produced in the lightedark box test. VUF 8430 reversed the scopolamine-induced amnesia in the passive avoidance test and showed anorexant activity in food deprived mice. Conversely, the H4R activation did not modify the immobility time in the tail suspension test. Rotarod performance test was employed to demonstrate that the effects observed following the administration of VUF 8430 and JNJ 10191584 were not due to impaired motor function of animals. Furthermore, both compounds did not alter spontaneous mobility and exploratory activity in the hole board test. These results show the antinociceptive, antiamnesic, anxiolytic and anorexant effects induced by neuronal H4R agonism, suggesting that H4 modulators may have broader utility further the control of inflammatory and immune processes.

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“…Instead it is more likely that the 5-HT 2C polymorphism predisposes individuals to weight gain via an unknown mechanism. The mechanism(s) by which H 1 -histamine antagonism might induce weight gain are currently unknown, although prior studies have amply demonstrated that H 1 -histamine receptor antagonism increases feeding in rodents whereas H 2 -histamine antagonism does not (Sakata et al, 1988;Fukagawa et al, 1989). Additionally, depletion of neuronal histamine increases feeding (Menon et al, 1971;Sakai et al, 1995).…”

Section: Discussionmentioning

confidence: 99%

H1-Histamine Receptor Affinity Predicts Short-Term Weight Gain for Typical and Atypical Antipsychotic Drugs

Kroeze

Hufeisen

Popadak

et al. 2003

Neuropsychopharmacol

698

494

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As a result of superior efficacy and overall tolerability, atypical antipsychotic drugs have become the treatment of choice for schizophrenia and related disorders, despite their side effects. Weight gain is a common and potentially serious complication of some antipsychotic drug therapy, and may be accompanied by hyperlipidemia, hypertension and hyperglycemia and, in some extreme cases, diabetic ketoacidosis. The molecular mechanism(s) responsible for antipsychotic drug-induced weight gain are unknown, but have been hypothesized to be because of interactions of antipsychotic drugs with several neurotransmitter receptors, including 5-HT 2A and 5-HT 2C serotonin receptors, H 1 -histamine receptors, a 1 -and a 2 -adrenergic receptors, and m3-muscarinic receptors. To determine the receptor(s) likely to be responsible for antipsychotic-drug-induced weight gain, we screened 17 typical and atypical antipsychotic drugs for binding to 12 neurotransmitter receptors. H 1 -histamine receptor affinities for this group of typical and atypical antipsychotic drugs were significantly correlated with weight gain (Spearman r ¼ À0.72; po0.01), as were affinities for a 1A adrenergic (r ¼ À0.54; po0.05), 5-HT 2C (r ¼ À0.49; po0.05) and 5-HT 6 receptors (r ¼ À0.54; po0.05), whereas eight other receptors' affinities were not. A principal components analysis showed that affinities at the H 1 , a 2A , a 2B , 5-HT 2A , 5-HT 2C , and 5-HT 6 receptors were most highly correlated with the first principal component, and affinities for the D 2 , 5-HT 1A , and 5-HT 7 receptors were most highly correlated with the second principal component. A discriminant functions analysis showed that affinities for the H 1 and a 1A receptors were most highly correlated with the discriminant function axis. The discriminant function analysis, as well as the affinity for the H 1 -histamine receptor alone, correctly classified 15 of the 17 drugs into two groups; those that induce weight gain and those that do not. Because centrally acting H 1 -histamine receptor antagonists are known to induce weight gain with chronic use, and because H 1 -histamine receptor affinities are positively correlated with weight gain among typical and atypical antipsychotic drugs, it is recommended that the next generation of atypical antipsychotic drugs be screened to avoid H 1 -histamine receptors.

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Blockade of the histamine H1-receptor in the rat ventromedial hypothalamus and feeding elicitation

Cited by 130 publications

References 12 publications

Proline Decreases the Suppressive Effect of Histidine on Food Intake and Fat Accumulation

Proline Decreases the Suppressive Effect of Histidine on Food Intake and Fat Accumulation

Pleiotropic effect of histamine H4 receptor modulation in the central nervous system

H1-Histamine Receptor Affinity Predicts Short-Term Weight Gain for Typical and Atypical Antipsychotic Drugs

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