ArticleMolecular psychiatry2022
Identification of an endocannabinoid gut-brain vagal mechanism controlling food reward and energy homeostasis.
Article in Molecular psychiatry, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 47 citations in OpenAlex.
- Probiotic-Mediated Vitamin D Supplementation Improves the Gut Microbiota and Vitamin D Receptor Composition in Obese Rats.Food science & nutrition · 2026Article
- PET Molecular Imaging of the Endocannabinoid System in Psychiatric Disorders.Neuroscience bulletin · 2026Review
- The gut-brain vagal axis governs mesolimbic dopamine dynamics and reward events.Science advances · 2026Article
- Exercise modulates food reward: neurobiological mechanisms and implications for weight management.Frontiers in nutrition · 2026Review
- CBMolecular psychiatry · 2026Article
- Striatal astrocytes modulate behavioral flexibility and whole-body metabolism in mice.Nature communications · 2025Article
- TLR4-dependent neuroinflammation mediates LPS-driven food-reward alterations during high-fat exposure.Journal of neuroinflammation · 2024Article
- Harnessing the Gut Microbiome: To What Extent Can Pre-/Probiotics Alleviate Immune Activation in Autism Spectrum Disorder?Nutrients · 2024Review
- Cholinergic Neurotransmission Controls Orexigenic Endocannabinoid Signaling in the Gut in Diet-Induced Obesity.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024Article
- NAPE-PLD in the ventral tegmental area regulates reward events, feeding and energy homeostasis.Molecular psychiatry · 2024Article
- The gut-brain axis and cognitive control: A role for the vagus nerve.Seminars in cell & developmental biology · 2024Review
- Spinal afferent neurons: emerging regulators of energy balance and metabolism.Frontiers in molecular neuroscience · 2024Review
- Differential exposure to palatable food and its effects on binge-like eating behavior in adolescent rats.Frontiers in psychology · 2024Article
- Anandamide and 2-arachidonoylglycerol baseline plasma concentrations and their clinical correlate in gambling disorder.European psychiatry : the journal of the Association of European Psychiatrists · 2023Article
- Association of anandamide and 2-arachidonoylglycerol concentrations with clinical features and body mass index in eating disorders and obesity.European psychiatry : the journal of the Association of European Psychiatrists · 2023Article
- The Role of the Endocannabinoid System in Binge Eating Disorder.International journal of molecular sciences · 2023Review
- Obese-associated gut microbes and derived phenolic metabolite as mediators of excessive motivation for food reward.Microbiome · 2023Article
- Metabolic Messengers: endocannabinoids.Nature metabolism · 2022Review
- Molecular Alterations of the Endocannabinoid System in Psychiatric Disorders.International journal of molecular sciences · 2022Review
- Gut microbes and food reward: From the gut to the brain.Frontiers in neuroscience · 2022Review
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The regulation of food intake, a sine qua non requirement for survival, thoroughly shapes feeding and energy balance by integrating both homeostatic and hedonic values of food. Unfortunately, the widespread access to palatable food has led to the development of feeding habits that are independent from metabolic needs. Among these, binge eating (BE) is characterized by uncontrolled voracious eating. While reward deficit seems to be a major contributor of BE, the physiological and molecular underpinnings of BE establishment remain elusive. Here, we combined a physiologically relevant BE mouse model with multiscale in vivo approaches to explore the functional connection between the gut-brain axis and the reward and homeostatic brain structures. Our results show that BE elicits compensatory adaptations requiring the gut-to-brain axis which, through the vagus nerve, relies on the permissive actions of peripheral endocannabinoids (eCBs) signaling. Selective inhibition of peripheral CB1 receptors resulted in a vagus-dependent increased hypothalamic activity, modified metabolic efficiency, and dampened activity of mesolimbic dopamine circuit, altogether leading to the suppression of palatable eating. We provide compelling evidence for a yet unappreciated physiological integrative mechanism by which variations of peripheral eCBs control the activity of the vagus nerve, thereby in turn gating the additive responses of both homeostatic and hedonic brain circuits which govern homeostatic and reward-driven feeding. In conclusion, we reveal that vagus-mediated eCBs/CB1R functions represent an interesting and innovative target to modulate energy balance and counteract food-reward disorders.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.