Cited by 431Biochemical Analysis and Sensing TechniquesNeurotransmitter Receptor Influence on BehaviorRegulation of Appetite and Obesity

Food Reward in the Absence of Taste Receptor Signaling

Open access
de Araujo, Ivan E., Oliveira-Maia, Albino J., Sotnikova, Tatyana D., Gainetdinov, Raul R., Caron, Marc G., Nicolelis, Miguel A.L., Simon, Sidney A.·2008·Neuron

Abstract

Food palatability and hedonic value play central roles in nutrient intake. However, postingestive effects can influence food preferences independently of palatability, although the neurobiological bases of such mechanisms remain poorly understood. Of central interest is whether the same brain reward circuitry that is responsive to palatable rewards also encodes metabolic value independently of taste signaling. Here we show that trpm5-/- mice, which lack the cellular machinery required for sweet taste transduction, can develop a robust preference for sucrose solutions based solely on caloric content. Sucrose intake induced dopamine release in the ventral striatum of these sweet-blind mice, a pattern usually associated with receipt of palatable rewards. Furthermore, single neurons in this same ventral striatal region showed increased sensitivity to caloric intake even in the absence of gustatory inputs. Our findings suggest that calorie-rich nutrients can directly influence brain reward circuits that control food intake independently of palatability or functional taste transduction.

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Crossref · 10.1016/j.neuron.2008.01.032

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  • Even when all taste processing is eliminated by genetic manipulation, mice still learn to prefer sugar over water.

    “But even when all taste processing is eliminated by genetic manipulation, mice still learn to prefer sugar over water, suggesting the generation of food reward by processes of glucose utilization ([44](#B44)).”

    From Food reward, hyperphagia, and obesity (2011) · cites this paper as [44]

  • The generation of food reward can occur by processes of glucose utilization.

    “suggesting the generation of food reward by processes of glucose utilization ([44](#B44)).”

    From Food reward, hyperphagia, and obesity (2011) · cites this paper as [44]

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References 39 · Cited by 431

Authors
de Araujo, I. E., Oliveira-Maia, A. J., Sotnikova, T. D., Gainetdinov, R. R., Caron, M. G., Nicolelis, M. A. L., & Simon, S. A.
Affiliations
  • Universidade do Porto (PT)
  • Duke Medical Center (US)
Venue
Neuron
Publisher
Elsevier BV
Published
2008-03
Volume
57
Issue
6
Pages
930-941
ISSN
0896-6273 (ISSN-L)
OpenAlex
W2046460103
Cited by
431
References
39
Citations by year
2026: 12 · 2025: 23 · 2024: 13 · 2023: 20 · 2022: 18 · 2021: 27 · 2020: 30 · 2019: 13 · 2018: 20 · 2017: 24 · 2016: 32 · 2015: 23 · 2014: 23 · 2013: 28 · 2012: 37
FWCI
27.82
Type
journal article
Language
en
Open access
Locations
  • Neuron (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • Philip Morris International
  • Fundació Catalana de Trasplantament
  • National Institutes of Health (DC-01065)
Topics
  • Health Sciences › Nursing › Nutrition and Dietetics › Biochemical Analysis and Sensing Techniques
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
  • Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Regulation of Appetite and Obesity
Keywords
food reward, calorific value, sucrose intake, dopamine release, ventral striatum, single-unit recording, food preferences, gustatory signaling
MeSH terms
Action Potentials, Analysis of Variance, Animals, Behavior, Animal, Blood Glucose, Choice Behavior, Conditioning, Operant, Dopamine, Dose-Response Relationship, Drug, Food Preferences, Male, Mice, Inbred C57BL, Neurons, Nucleus Accumbens, Reward, Stimulation, Chemical, Sucrose, Sweetening Agents, Signal Transduction, Mice, Knockout, Statistics, Nonparametric, TRPM Cation Channels, Mice

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