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Insulin, leptin and reward
Open accessAbstract
Feeding for pleasure, or "non-homeostatic feeding", potentially contributes to the rapid development of obesity worldwide. Obesity is associated with an imbalance of regulatory hormones which normally act to maintain stable energy balance and body weight. The adiposity hormones insulin and leptin are two such signals elevated in obesity with the capacity to dampen feeding behavior through their action on hypothalamic circuits which regulate appetite and metabolism. Recent evidence suggests that both hormones achieve this degree of regulation by inhibiting the rewarding aspects of feeding behavior, perhaps by signaling within midbrain reward circuits. This review describes the capacity of both insulin and leptin to regulate reward-related behavior.
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“juxtaposed interventions that decrease BMI and reduce plasma levels of insulin and leptin enhance the sensitivity to psychostimulant drugs (39).”
From Obesity and addiction: Neurobiological overlaps (2013) · cites this paper as [39]
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“Moreover, interventions that decrease BMI and reduce plasma levels of insulin and leptin enhance the sensitivity to psychostimulant drugs (25),”
From The Addictive Dimensionality of Obesity (2013) · cites this paper as [25]
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“Furthermore, insulin and leptin appear to negatively modulate the food rewarding system [67], whereas ghrelin exerts opposite effects [68]; the changes in these hormonal concentrations following sleep restriction could therefore contribute to the increased hedonic, rather than homeostatic, eating, that may be typical of short sleepers.”
From Role of sleep duration in the regulation of glucose metabolism and appetite (2010) · cites this paper as [67]
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Metadata
- Authors
- Davis, J. F., Choi, D. L., & Benoit, S. C.
- Affiliations
- University of Cincinnati (US)
- Corresponding author
- Davis, Jon F.
- Choi, Derrick L.
- Benoit, Stephen C.
- ORCID
- Davis, Jon F.
- Venue
- Trends in Endocrinology & Metabolism
- Publisher
- Elsevier BV
- Published
- 2010-02
- Volume
- 21
- Issue
- 2
- Pages
- 68-74
- ISSN
- 1043-2760 (ISSN-L)
- PMC
- PMC2822063
- OpenAlex
- W2011386410
- Cited by
- 129
- References
- 75
- Citations by year
- 2026: 4 · 2025: 7 · 2024: 8 · 2023: 2 · 2022: 10 · 2021: 4 · 2020: 4 · 2019: 8 · 2018: 3 · 2017: 9 · 2016: 7 · 2015: 7 · 2014: 10 · 2013: 16 · 2012: 10
- FWCI
- 1.06
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Trends in Endocrinology and Metabolism (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institute of Diabetes and Digestive and Kidney Diseases (P01DK056863)
- 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
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Adipokines, Inflammation, and Metabolic Diseases
- Keywords
- insulin, leptin, reward, obesity, appetite regulation, hypothalamic circuits, energy balance, feeding behavior
- MeSH terms
- Animals, Appetite Regulation, Central Nervous System, Feeding Behavior, Homeostasis, Humans, Insulin, Limbic System, Models, Biological, Reward, Leptin
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