Abstract
Our survival relies on the ability to search for food to attend immediate metabolic needs and to store excess energy in the form of fat to meet metabolic demands during fasting. Hunger and satiety are key factors driving eating behavior and are under control of a complex interplay of several central and peripheral neuroendocrine systems. Interest in the control of feeding has increased as a result of the obesity epidemic and rising incidence of metabolic diseases. The first evidence of the involvement of brain histaminergic system in the regulation of feeding dates back to the 1970s. Since then, many studies ensued, and up-to-date evidence suggests an inverse relationship between neuronal histamine and food intake. Preclinical studies demonstrated that brain histamine is released during both the appetitive and consummatory phases of feeding behavior and is also involved in the control of peripheral mechanisms regulating energy expenditure. Hypothalamic H1 and H3 receptors are crucial for the regulation of the diurnal rhythm of food consumption; furthermore, these receptors have been specifically recognized as mediators of energy intake and expenditure. All these features point for the histaminergic system as an attractive target for the development of new anti-obesity drugs. Unfortunately, so far, no selective brain-penetrating H1 receptor agonists have been identified, and clinical trials of the potential H3 receptor antagonists-induced weight loss did not meet up to the expectations or were interrupted. Not all is lost tough, recent clinical trials demonstrated the potential of betahistine (an H1 agonist/H3 antagonist) in opposing metabolic side effects associated with chronic antipsychotic treatment.
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