Involvement of the Histaminergic System in Leptin-Induced Suppression of Food Intake

Morimoto, Tadatsugu; Yamamoto, Yumiko; Mobarakeh, Jalal Izadi; Yanai, Kazuhiko; Watanabe, Takehiko; Watanabe, Takeshi; Yamatodani, Atsushi

doi:10.1016/s0031-9384(99)00123-7

Cited by 103 publications

(56 citation statements)

References 30 publications

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“…It is fundamental for appetitive and aversive responses during motivated behavior (24), and blockade of histamine H 1 R in the hypothalamus is believed to be responsible for the weight gain and metabolic dysregulation associated with the clinical use of atypical antipsychotics (25). Several peptides and hormonessuch as leptin, corticotropin-, TSH-releasing hormones, and nefastin-1-are satiety modulators acting, at least in part, through histamine neurons activity (26)(27)(28). So far, there has been no information regarding brain histamine taking part in the anorexic effects of a modulator that, at the dose used in this study, does not easily pass the blood-brain barrier.…”

Section: Discussionmentioning

confidence: 99%

Satiety factor oleoylethanolamide recruits the brain histaminergic system to inhibit food intake

Provensi

Coccurello

Umehara

et al. 2014

Proc. Natl. Acad. Sci. U.S.A.

108

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Key factors driving eating behavior are hunger and satiety, which are controlled by a complex interplay of central neurotransmitter systems and peripheral stimuli. The lipid-derived messenger oleoylethanolamide (OEA) is released by enterocytes in response to fat intake and indirectly signals satiety to hypothalamic nuclei. Brain histamine is released during the appetitive phase to provide a high level of arousal in anticipation of feeding, and mediates satiety. However, despite the possible functional overlap of satiety signals, it is not known whether histamine participates in OEA-induced hypophagia. Using different experimental settings and diets, we report that the anorexiant effect of OEA is significantly attenuated in mice deficient in the histamine-synthesizing enzyme histidine decarboxylase (HDC-KO) or acutely depleted of histamine via interocerebroventricular infusion of the HDC blocker α-fluoromethylhistidine (α-FMH). α-FMH abolished OEA-induced early occurrence of satiety onset while increasing histamine release in the CNS with an H 3 receptor antagonist-increased hypophagia. OEA augmented histamine release in the cortex of fasted mice within a time window compatible to its anorexic effects. OEA also increased c-Fos expression in the oxytocin neurons of the paraventricular nuclei of WT but not HDC-KO mice. The density of c-Fos immunoreactive neurons in other brain regions that receive histaminergic innervation and participate in the expression of feeding behavior was comparable in OEA-treated WT and HDC-KO mice. Our results demonstrate that OEA requires the integrity of the brain histamine system to fully exert its hypophagic effect and that the oxytocin neuron-rich nuclei are the likely hypothalamic area where brain histamine influences the central effects of OEA.histamine receptors | behavioral satiety sequence | BSS | paraventricular hypothalamic nuclei | PVN E ating behavior is regulated by central neurotransmitter systems and peripheral stimuli that interact to change the behavioral state and concur to alter homeostatic aspects of appetite and energy expenditure. The fatty acid amide oleoylethanolamide (OEA) is released by the small intestine in a stimulus-dependent manner and suppresses food intake by activating peroxisome proliferator-activated receptor-α (PPAR-α) (1). Systemic administration of OEA induces c-Fos mRNA expression through the vagus nerve to the nucleus of the solitary tract (NST), supraoptic nuclei (SON), and paraventricular hypothalamic nuclei (PVN) and increases the expression of oxytocin (2, 3), which is involved in the central coordination of homeostatic signals and feeding behavior (4). However, it is not known whether OEA recruits other neurotransmitter systems in the brain to reduce food intake. Histaminergic neurons are clustered in the hypothalamic tuberomammillary nuclei (TMN). They send projections organized in functionally distinct circuits impinging on different brain regions (5), and their firing frequency changes according to the behavioral state (6). Brain histamin...

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Section: Discussionmentioning

confidence: 99%

Satiety factor oleoylethanolamide recruits the brain histaminergic system to inhibit food intake

Provensi

Coccurello

Umehara

et al. 2014

Proc. Natl. Acad. Sci. U.S.A.

108

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“…Furthermore, either 2-AG injections in the shell of the NAcc [70], or anandamide administration into the VMH induce hyperfagia [71]. In some aspect, the histaminergic and endocannabinoid systems seem to be regulated in an opposing fashion: for instance, systemic administration of leptin that signals to the hypothalamus the nutritional state and reduces food intake, facilitates histamine release from the hypothalamus [72], whereas it downregulates endocannabinoids levels in the same region [73]. Furthermore, concentrations of hypothalamic histamine and tele-methylhistamine, a major histamine metabolite, are significantly lower in obese (ob/ob) and diabetic (db/db) mice, and fatty ( fa/ fa) rats, leptin-deficient and leptin-receptor defective animals, respectively, relative to lean littermates [54].…”

Section: Endocannabinoids and Feeding Behaviormentioning

confidence: 99%

Histamine in the brain: Beyond sleep and memory

Passani¹,

Giannoni²,

Bucherelli

et al. 2007

Biochemical Pharmacology

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“…HDC gene knock-out mice lack histamine almost completely (4). Inhibition of histamine synthesis in mice, by treatment with an HDC inhibitor or by an HDC gene knock-out, alters the histaminergic neuron-mediated physiological responses, including arousal (5,6), appetite (7), and locomotor activity (8,9). Tourette syndrome, a developmental neuropsychiatric disorder, is related to an HDC gene mutation (10).…”

mentioning

confidence: 99%

Structural Study Reveals That Ser-354 Determines Substrate Specificity on Human Histidine Decarboxylase

Kakemoto

Nitta

Ueno

et al. 2012

Journal of Biological Chemistry

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Background: HDC catalyzes the rate-limiting step in histamine biosynthesis. Results: A mutation based on the crystal structure of HDC changed the substrate selectivity from L-histidine to L-DOPA. Conclusion: The molecular basis for substrate specificity and recognition of group II PLP-dependent decarboxylases were clarified. Significance: Knowledge of the HDC tertiary structure now makes it possible to design novel drugs that prevent histamine biosynthesis.

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Involvement of the Histaminergic System in Leptin-Induced Suppression of Food Intake

Cited by 103 publications

References 30 publications

Satiety factor oleoylethanolamide recruits the brain histaminergic system to inhibit food intake

Satiety factor oleoylethanolamide recruits the brain histaminergic system to inhibit food intake

Histamine in the brain: Beyond sleep and memory

Structural Study Reveals That Ser-354 Determines Substrate Specificity on Human Histidine Decarboxylase

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