The role of endocannabinoids in the control of eating disorders

Abstract

Eating Disorder (ED) is a syndrome characterized by persistent alteration of eating behavior and the conditions that cause an insufficient ingestion and/or adsorption of foods. There are three different ED diseases: Anorexia Nervosa (AN), Bulimia Nervosa (BN) and Binge Eating Disorders (BED). ED are complex conditions that arise from a combination of long-standing behavioral, emotional, psychological, interpersonal, and social factors. The neuronal circuits that control the ingestion of food are mainly related to catecholaminergic, serotoninergic and peptidergic systems. In this respect, while serotonin, dopamine and prostaglandin promote the ingestion of food, by contrast, neuropeptide Y, norepinephrine, GABA and opioid peptides inhibit food ingestion thus causing the occurrence of ED. The drugs mainly used in the treatment of ED are antidepressants such as selective serotonin reuptake inhibitors and tricyclic antidepressant. Additionally, mood stabilizers (lithium), anxiolytics, serotonin and noradrenalin reuptake inhibitors and antipsychotic drugs are often used in the treatment of ED.Several studies indicate that the endocannabinoid system is involved in ED supporting the idea that the cannabinoid signaling system is a key modulatory element in the activity in the brain area associated with ED.

The Role of the Endocannabinoid System in Binge Eating Disorder

“…Although several components of the ECS may be involved, CB1 receptors appear crucial for the central and peripheral effects of cannabinoids on eating behavior [26]. CB1 receptors are widely expressed in reward-related brain regions [14], initially suggesting a role in the motivation to eat [26]. A well-known example of THC's effect on eating behavior is marijuana-induced "munchies".…”

“…In addition to its involvement in appetite regulation and reward-based eating, several investigations indicate that the ECS is involved in many aspects of eating disorders and obesity [3,26,114]. Interestingly, studies in patients with psychiatric conditions have revealed relationships between ECS gene polymorphisms and their pathological state [114].…”

Pharmacophore-based Virtual Screening From Phytocannabinoids for Anti-obesity Activity

“…If it is presynaptic and with adenylate Cyclase inhibition, it may be generated hyperpolarization with a consequent decrease in neurotransmitter release. If it is postsynaptic, the action of rCB1 is on K + channel regulation and adenylate cyclase inhibition [7,9]. The neuromodulatory action of AEA is due to the following characteristics: they have distinct synthetic pathways; their cell release occurs after membrane depolarization and calcium intake; and its action is terminated with its reuptake and degradation by an intracellular enzyme (fatty acid amide hydrolase) [10].…”