title: Endocannabinoids and energy homeostasis: an update.
abstract: The endocannabinoid system (ECS) is a widespread intercellular signaling system that plays a critical role in energy homeostasis, meant as the precise matching of caloric intake with energy expenditure which normally keeps body weight stable over time. Complex interactions between environmental and neurohormonal systems directly contribute to the balance of energy homeostasis. This review highlights established and more recent data on the brain circuits in which the ECS plays an important regulatory role, with focus on the hypothalamus, a region where numerous interacting systems regulating feeding, satiety, stress, and other motivational states coexist. Although not meant as an exhaustive review of the field, this article will discuss how endocannabinoid tone, in addition to reinforcing reward circuitries and modulating food intake and the salience of food, controls lipid and glucose metabolism in several peripheral organs, particularly the liver and adipose tissue. Direct actions in the skeletal muscle and pancreas are also emerging and are briefly discussed. This review provides new perspectives into endocannabinoid control of the neurochemical causes and consequences of energy homeostasis imbalance, a knowledge that might lead to new potential treatments for obesity and related morbidities.
authors.affiliation: Endocannabinoid Research Group, Institute of Biomolecular Chemistry, CNR, Pozzuoli, Italy.
authors.forename: Luigia
authors.initials: L
authors.lastname: Cristino
authors.forename: Thorsten
authors.initials: T
authors.lastname: Becker
authors.forename: Vincenzo
authors.initials: V
authors.lastname: Di Marzo
mesh_terms: D000818:Animals; D001069:Appetite Regulation; D050260:Carbohydrate Metabolism; D063388:Endocannabinoids / Q000502:physiology*; D002149:Energy Intake; D004734:Energy Metabolism; D006706:Homeostasis; D006801:Humans; D007031:Hypothalamus / Q000502:physiology; D050356:Lipid Metabolism
chemical_list: D063388:Endocannabinoids
keywords: anti-obesity drugs; hypothalamus; leptin; metabolic disfunctions; retrograde neurotransmission