histamine/obesity

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Bicyclic and tricyclic heterocycle derivatives as histamine H3 receptor antagonists for the treatment of obesity.

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A novel series of non-imidazole bicyclic and tricyclic histamine H3 receptor antagonists has been discovered. Compound 17 was identified as a centrally penetrant molecule with high receptor occupancy which demonstrates robust oral activity in rodent models of obesity. In addition compound 17

Histamine H1-receptors differentially mediate the action of amylin on hypothalamic neurons in control and in overweight rats.

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The hypothalamic arcuate, dorsomedial and paraventricular nuclei are involved in regulation of body weight and food intake and contain binding sites for the anorexigenic amylin. Effects of amylin on medial arcuate and paraventricular neurons studied in adult rats overweight through early postnatal

Histamine H3 receptor antagonists: preclinical promise for treating obesity and cognitive disorders.

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The histamine H3 receptor is an attractive G protein-coupled receptor drug target that regulates neurotransmission in the central nervous system and plays a role in cognitive and homeostatic functions. Drug discovery efforts by numerous pharmaceutical companies have focused on the preclinical

Novel Tetrahydroquinazolinamines as Selective Histamine 3 Receptor Antagonists for the Treatment of Obesity.

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The histamine 3 receptor (H3R) is a presynaptic receptor, which modulates several neurotransmitters including histamine and various essential physiological processes, such as feeding, arousal, cognition, and pain. The H3R is considered as a drug target for the treatment of several central nervous

KSK19 - Novel histamine H3 receptor ligand reduces body weight in diet induced obese mice.

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AIMS

Histamine H₃ receptors ligands act anorectic by blocking the H₃ autoreceptors in the CNS, that results in increased synthesis and disinhibition of histamine release. Histamine further influencing H₁ receptors participates in the

Comparison of the effect of an H(3)-inverse agonist on energy intake and hypothalamic histamine release in normal mice and leptin resistant mice with high fat diet-induced obesity.

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Leptin is a key signal linking peripheral adiposity levels to the regulation of energy homeostasis in the brain. The injection of leptin decreases body weight and food intake in lean rodents; however, in a rodent model of high fat diet-induced obesity (DIO), the exogenous leptin cannot improve

Hypothalamic neuronal histamine in genetically obese animals: its implication of leptin action in the brain.

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Leptin regulates feeding behavior and energy metabolism by affecting hypothalamic neuromodulators. The present study was designed to examine hypothalamic neuronal histamine, a recently identified mediator of leptin signaling in the brain, in genetic obese animals. Concentrations of hypothalamic

Targeted disruption of H3 receptors results in changes in brain histamine tone leading to an obese phenotype.

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Histamine is an aminergic neurotransmitter that is localized in the CNS and in peripheral tissues. To date, four histamine receptors have been identified, and the H3 receptor, which was recently cloned, is predominantly expressed in the CNS. The peripheral functions of histamine have been

Increased susceptibility to diet-induced obesity in histamine-deficient mice.

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OBJECTIVE The neurotransmitter histamine is involved in the regulation of appetite and in the development of age-related obesity in mice. Furthermore, histamine is a mediator of the anorexigenic action of leptin. The aim of the present study was to investigate a possible role of histamine in the

Molecular mechanisms of neuronal histamine and its receptors in obesity.

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Obesity is an important health problem because it is associated with diseases such as type 2 diabetes, hypertension, and hyperlipidemia in metabolic syndrome. The detail molecular mechanisms that underlie obesity have not been fully elucidated, and its therapeutic approach is of general interest.

Neuronal histamine regulates food intake, adiposity, and uncoupling protein expression in agouti yellow (A(y)/a) obese mice.

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Hypothalamic neuronal histamine and its H(1) receptor (H(1)-R) form a part of the leptin-signaling pathway in the brain and have been shown to regulate body weight and adiposity in diabetic (db/db) and diet-induced obese mice by affecting food intake and uncoupling protein mRNA expression. The

Zucker obese rats: defect in brain histamine control of feeding.

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Manipulation of hypothalamic histamine produced different effects on feeding between the Zucker obese (fa/fa) and their lean littermate rats (Fa/-). Infusion of a histamine H1-receptor antagonist into the third cerebroventricle elicited feeding in the lean and Wistar King A rats, but it did not

Neuronal histamine and its receptors: implication of the pharmacological treatment of obesity.

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Obesity is the effect of imbalance between energy intake and expenditure and forms a fundamental basis of the metabolic syndrome. A number of substances implicated in the regulation of energy metabolism represent opportunities for anti-obesity drug development. Neuronal histamine and its receptors

Central Histamine, The H3-Receptor and Obesity Therapy.

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The brain histaminergic system plays a pivotal role in energy homeostasis, through H1-receptor activation, it increases the hypothalamic release of histamine that decreases food intake and reduces body weight. One way to increase the release of hypothalamic histamine is through the use of

Therapeutic approach of histamine H3 receptors in obesity.

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Obesity is considered one of the risk factors for metabolic disorders. There is increasing evidence that obesity is under control of several cytokines and hormone in the brain. Brain histamine and H3 receptors are important factors for regulating obesity. The results of physiological and

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