The histaminergic system as a target for the prevention of obesity and metabolic syndrome

Provensi, Gustavo; Blandina, Patrizio; Passani, Maria Beatrice

doi:10.1016/j.neuropharm.2015.07.002

Cited by 61 publications

(50 citation statements)

References 132 publications

(128 reference statements)

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“…It has also been reported that SGAs such as olanzapine can directly modulate histaminergic neurotransmission in the hypothalamus, which correlated with the regulation of feeding behaviour in rats [50]. Therefore, the histaminergic system could be a target for preventing obesity and other metabolic disorders [33].…”

Section: Methodsmentioning

confidence: 97%

“…The neurotransmitter histamine plays a crucial role in the regulation of a wide range of behavioural and physiological functions in humans and animals, such as appetite, drinking, sleep, wakefulness, locomotor activity, learning and memory [37,34,42,33]. In particular, histamine has been implicated in the regulation of energy homeostasis [12,43,44].…”

Section: Methodsmentioning

confidence: 99%

“…Therefore, it is important to investigate the potential for targeting these receptors to control SGA-induced weight gain. In view that histaminergic system could be a target for preventing obesity [33], this paper reviewed recent reports from both animal and clinical studies on exploring the potential of betahistine (an H 1 R agonist and H 3 receptor (H 3 R) antagonist) to ameliorate SGA-induced weight gain/obesity, and more importantly summarized recent progresses in the underlying mechanisms for this preventing effects by betahistine co-treatment.…”

Section: Introductionmentioning

confidence: 99%

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Ameliorating antipsychotic-induced weight gain by betahistine: Mechanisms and clinical implications

Lian

Huang

Pai

et al. 2016

Pharmacological Research

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Second generation antipsychotic drugs (SGAs) cause substantial body weight gain/obesity and other metabolic side-effects such as dyslipidaemia. Their antagonistic affinity to the histaminergic H1 receptor (H1R) has been identified as one of the main contributors to weight gain/obesity side-effects. The effects and mechanisms of betahistine (a histaminergic H1R agonist and H3 receptor antagonist) have been investigated for ameliorating SGA-induced weight gain/obesity in both animal models and clinical trials. It has been demonstrated that co-treatment with betahistine is effective in reducing weight gain, associated with olanzapine in drug-naïve patients with schizophrenia, as well as in the animal models of both drug-naïve rats and rats with chronic, repeated exposure to olanzapine. Betahistine co-treatment can reduce food intake and increase the effect of thermogenesis in brown adipose tissue by modulating hypothalamic H1R-NPY-AMPKα (NPY: neuropeptide Y; AMPKα: AMP-activated protein kinase α) pathways, and ameliorate olanzapineinduced dyslipidaemia through modulation of AMPKα-SREBP-1-PPARα-dependent pathways (SREBP-1: Sterol regulatory element binding protein 1; PPARα: Peroxisome proliferator-activated receptor-α) in the liver. Although reduced locomotor activity was observed from antipsychotic treatment in rats, betahistine did not affect locomotor activity. Importantly, betahistine co-treatment did not influence the effects of antipsychotics on serotonergic receptors in the key brain regions for antipsychotic therapeutic efficacy. However, betahistine co-treatment reverses the upregulated dopamine D2 binding caused by chronic olanzapine administration, which may be beneficial in reducing D2 supersensitivity often observed in chronic antipsychotic treatment. Therefore, these results provide solid evidence supporting further clinical trials in treating antipsychotics-induced weight gain using betahistine in patients with schizophrenia and other mental disorders.

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Section: Methodsmentioning

confidence: 97%

Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Ameliorating antipsychotic-induced weight gain by betahistine: Mechanisms and clinical implications

Lian

Huang

Pai

et al. 2016

Pharmacological Research

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“…One such pathway originates in the NST toward the digestive tract facilitating fat digestion and absorption (Figure 1). Another example of central control of peripheral functions is provided by the influence exerted by the hypothalamic histaminergic neurons, one of the key brain systems regulating eating behavior [96,97] on peripheral homeostatic responses. Preclinical studies showed that the administration of histamine or of an agonist of The Endocannabinoid-Like Derivative Oleoylethanolamide at the Gut-Brain Interface: A "Lipid Way" to Control Energy Intake and Body Weight http://dx.doi.org/10.5772/63147 the histamine H 1 receptor in the ventricle or the hypothalamic paraventricular nucleus, where activation of these receptors induces satiety, increases mRNA expression levels of uncoupling protein 1 (Ucp1), a marker of energy expenditure, in brown adipose tissue and increases the electrophysiological activity of sympathetic nerves that innervate it [98,99].…”

Section: The Notion Of Brain-gut Interfacementioning

confidence: 99%

The Endocannabinoid-Like Derivative Oleoylethanolamide at the Gut–Brain Interface: A “Lipid Way” to Control Energy Intake and Body Weight

Passani¹,

Coccurello²

2016

Cannabinoids in Health and Disease

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In the last three decades, we witnessed a concomitant major increase in lifespan and a worldwide increasing incidence of chronic diseases such as obesity and type 2 diabetes. Disruption of energy homeostasis and systemic inflammation appear as common traits of these epidemic human diseases. The conventional endocannabinoid (eCB) system encompasses two G-protein-coupled receptors (GPCRs), their endogenous ligands (anandamide and 2-AG), and the enzymes essential for eCB biosynthesis and hydrolytic inactivation. Nonetheless, the family of eCB-like derivatives is growing constantly including other N-acylethanolamines (NAEs) and 2-monoacylglycerols (2-MAGs) that do not bind canonical CB receptors rather other orphan G-protein-coupled receptors or peroxisome proliferator-activated nuclear receptors (PPARs). Here, we focus on the recent knowledge gathered on one such PPAR endocannabinoid ligand, oleoylethanolamide (OEA), from the identification of its synthesis in the small intestine to its anorexiant function with particular emphasis on our discovery of the main brain neurotransmitters system involved in its satiating effects.

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“…26 Recently, manyhuman studies are starting to provide evidence that the pharmacological manipulation of the histaminergic system influences weight gain and body mass index. 27 Betahistine is an anti-vertigo drug, commonly prescribed to patients with balance disorders or to improve vertigo symptoms associated with Meniere's disease. Betahistine has two modes of action.…”

mentioning

confidence: 99%

Role of betahistine in glycemic control of obese subjects: a placebo- controlled clinical trial

Al-Anbari

Sahib

Al-Mukhtar

2016

Int J Basic Clin Pharmacol

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Background: Poor glycemic control, insulin resistance and abnormal beta cell function are of the most important complications that associated with obesity, targeting of such complications with pharmacological agents depending on the already existing central mechanism may decrease the incidence of morbidity and mortality among obese subjects. Betahistine is an anti-vertigo drug, commonly prescribed to patients with balance disorders or to improve vertigo symptoms associated with Meniere's disease. The aim of this study was to investigate the effect of betahistine on glycemic status, insulin resistance and pancreatic function in obese subjects.Methods: A randomized, placebo controlled trial was carried out on 72 obese subjecta of both sexes with age range of 18-50 years who allocated into two groups: Group A: 48 patients treated with 144mg /day in three divided every eight hours for twelve weeks. Group B: 24 patients treated with placebo for twelve weeks to serve as control. For each group, demographic data, liver and renal function tests beside the studied parameters were investigated at baseline and after 12 weeks.Results: Administration of betahistine to obese subjects resulted in improvement in fasting blood glucose, glycosylated hemoglobin, insulin resistance and beta cell percent values after twelve weeks compared to baseline values and placebo treated group.Conclusions: Administration of betahistine in a dose of 144mg /day for twelve weeks to obese subjects effectively improve glycemic control, insulin resistance and beta cell functions in these subjects, indicating the beneficial effect of betahistine in slowing or reversing the long term progress of obesity complications without incidence of any serious adverse effects, indicating its efficacy and safety.

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The histaminergic system as a target for the prevention of obesity and metabolic syndrome

Cited by 61 publications

References 132 publications

Ameliorating antipsychotic-induced weight gain by betahistine: Mechanisms and clinical implications

Ameliorating antipsychotic-induced weight gain by betahistine: Mechanisms and clinical implications

The Endocannabinoid-Like Derivative Oleoylethanolamide at the Gut–Brain Interface: A “Lipid Way” to Control Energy Intake and Body Weight

Role of betahistine in glycemic control of obese subjects: a placebo- controlled clinical trial

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