Insulin, leptin and reward

Davis, Jon F.; Choi, Derrick L.; Benoit, Stephen C.

doi:10.1016/j.tem.2009.08.004

Cited by 129Regulation of Appetite and ObesityNeurotransmitter Receptor Influence on BehaviorAdipokines, Inflammation, and Metabolic Diseases

Insulin, leptin and reward

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Davis, Jon F., Choi, Derrick L., Benoit, Stephen C.·2010·Trends in Endocrinology & Metabolism

DOI 10.1016/j.tem.2009.08.004PMC PMC2822063

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Abstract

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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Interventions that decrease BMI and reduce plasma levels of insulin and leptin enhance sensitivity to psychostimulant drugs.
“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]
Interventions that decrease BMI and reduce plasma insulin and leptin enhance sensitivity to psychostimulant drugs.
“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]
Insulin and leptin appear to negatively modulate the food rewarding system, whereas ghrelin exerts opposite effects.
“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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Energy regulatory signals and food reward
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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)
DOI: 10.1016/j.tem.2009.08.004
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
Licence: www.elsevier.com/tdm/userlicense/1.0/ (tdm)
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 › Epidemiology › 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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Insulin, leptin and reward

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