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The Role of the Endocannabinoid System in Eating Disorders: Neurochemical and Behavioural Preclinical Evidence

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The endocannabinoid system has long been known as a modulator of several physiological functions, among which the homeostatic and hedonic aspects of eating. CB1 receptors are widely expressed in brain regions that control food intake, reward and energy balance. Animal and human studies indicate that CB1 receptor agonists possess orexigenic effects enhancing appetite and increasing the rewarding value of food. Conversely, CB1 antagonists have been shown to inhibit the intake of food.

Eating disorders include a range of chronic and disabling related pathological illnesses that are characterized by aberrant patterns of feeding behaviour and weight regulation, and by abnormal attitudes and perceptions toward body shape image. The psychological and biological factors underlying eating disorders are complex and not yet completely understood. However in the last decades, converging evidence have led to hypothesise a link between defects in the endocannabinoid system and eating disorders, including obesity. Here we review the neurochemical and behavioural preclinical evidence supporting the role of the endocannabinoid system in eating disorders to offer the reader an update regarding the state of the art. Despite the recent withdrawal from the market of rimonabant for treating obesity and overweight individuals with metabolic complications due to its psychiatric side effects, preclinical findings support the rationale for the clinical development of drug which modulate the endocannabinoid system in the treatment of eating disorders.
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Keywords: CB1 receptors; Endocannabinoid system; anorexia nervosa; binge eating disorder; bulimia nervosa; eating disorders; food intake; obesity

Document Type: Research Article

Publication date: April 1, 2014

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    Each thematic issue of Current Pharmaceutical Design covers all subject areas of major importance to modern drug design, including: medicinal chemistry, pharmacology, drug targets and disease mechanism.
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