Reward mechanisms in obesity: new insights and future directions
Open accessAbstract
Food is consumed in order to maintain energy balance at homeostatic levels. In addition, palatable food is also consumed for its hedonic properties independent of energy status. Such reward-related consumption can result in caloric intake exceeding requirements and is considered a major culprit in the rapidly increasing rates of obesity in developed countries. Compared with homeostatic mechanisms of feeding, much less is known about how hedonic systems in brain influence food intake. Intriguingly, excessive consumption of palatable food can trigger neuroadaptive responses in brain reward circuitries similar to drugs of abuse. Furthermore, similar genetic vulnerabilities in brain reward systems can increase predisposition to drug addiction and obesity. Here, recent advances in our understanding of the brain circuitries that regulate hedonic aspects of feeding behavior will be reviewed. Also, emerging evidence suggesting that obesity and drug addiction may share common hedonic mechanisms will also be considered.
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Food is frequently used as a coping mechanism to manage emotional states, and highly palatable foods activate brain reward circuits in ways that parallel addictive behaviors.
“Food is frequently used as a coping mechanism to manage emotional states, and highly palatable foods, especially those high in sugar and fat, activate brain reward circuits in ways that parallel addictive behaviors.”
From Weight maintenance after discontinuation of GLP-1 therapies (2026) · cites this paper as [46]
The extended reward system involves regions associated with salience and cortical inhibition (prefrontal control) networks.
“The extended reward system involves regions associated with salience and cortical inhibition (prefrontal control) networks 39, 89, 90, 91.”
From History of early life adversity is associated with increased food addiction and sex-specific alterations in reward network connectivity in obesity (2019) · cites this paper as [90]
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- Authors
- Kenny, P. J.
- Affiliations
- Scripps Research Institute (US)
- Corresponding author
- Kenny, Paul J.
- ORCID
- Kenny, Paul J.
- Venue
- Neuron
- Publisher
- Elsevier BV
- Published
- 2011-02
- Volume
- 69
- Issue
- 4
- Pages
- 664-679
- ISSN
- 0896-6273 (ISSN-L)
- PMC
- PMC3057652
- OpenAlex
- W2065485036
- Cited by
- 748
- References
- 209
- Citations by year
- 2026: 24 · 2025: 33 · 2024: 34 · 2023: 39 · 2022: 34 · 2021: 58 · 2020: 85 · 2019: 49 · 2018: 54 · 2017: 51 · 2016: 46 · 2015: 64 · 2014: 61 · 2013: 47 · 2012: 45
- FWCI
- 5.76
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Neuron (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institute on Drug Abuse (R01DA025983)
- Topics
- Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Regulation of Appetite and Obesity
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
- Social Sciences › Psychology › Clinical Psychology › Eating Disorders and Behaviors
- Keywords
- obesity, food reward, hedonic feeding, brain reward system, palatable food, energy homeostasis, neural adaptation, drug addiction, genetic susceptibility, overeating
- MeSH terms
- Animals, Brain, Energy Metabolism, Feeding Behavior, Homeostasis, Humans, Models, Neurological, Obesity, Reward
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