Hungry brains: A meta-analytical review of brain activation imaging studies on food perception and appetite in obese individuals

•We provide the first quantitative assessment of neurocognitive theories of obesity.•These results were obtained with quantitative meta-analyses of fMRI studies.•Overall, we provide support for an incentive sensitization theory of obesity.•Obese individuals have greater activation of reward regions...

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Published inNeuroscience and biobehavioral reviews Vol. 94; pp. 271 - 285
Main Authors Devoto, F., Zapparoli, L., Bonandrini, R., Berlingeri, M., Ferrulli, A., Luzi, L., Banfi, G., Paulesu, E.
Format Journal Article
LanguageEnglish
Published United States Elsevier Ltd 01.11.2018
Subjects
Activation likelihood estimation
Animals
Appetite - physiology
Brain - diagnostic imaging
Brain - physiopathology
Food
Hierarchical clustering
Humans
Meta-analysis
Neuroimaging
Obesity
Obesity - diagnostic imaging
Obesity - physiopathology
Obesity - psychology
Perception - physiology
Reward system
CCA
Neuroimaging
OP
Obesity
VTA
Reward system
Activation likelihood estimation
CL
PFC
Hierarchical clustering
BP
HW
Meta-analysis
fMRI
OB
dlPFC
R-DVM
ALE
BOLD
HC
SN
PL
PET
BMI
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Abstract •We provide the first quantitative assessment of neurocognitive theories of obesity.•These results were obtained with quantitative meta-analyses of fMRI studies.•Overall, we provide support for an incentive sensitization theory of obesity.•Obese individuals have greater activation of reward regions for visual food cues.•The brain of obese individuals is more sensitive to hunger and less to satiety. The dysregulation of food intake in chronic obesity has been explained by different theories. To assess their explanatory power, we meta-analyzed 22 brain-activation imaging studies. We found that obese individuals exhibit hyper-responsivity of the brain regions involved in taste and reward for food-related stimuli. Consistent with a Reward Surfeit Hypothesis, obese individuals exhibit a ventral striatum hyper-responsivity in response to pure tastes, particularly when fasting. Furthermore, we found that obese subjects display more frequent ventral striatal activation for visual food cues when satiated: this continued processing within the reward system, together with the aforementioned evidence, is compatible with the Incentive Sensitization Theory. On the other hand, we did not find univocal evidence in favor of a Reward Deficit Hypothesis nor for a systematic deficit of inhibitory cognitive control. We conclude that the available brain activation data on the dysregulated food intake and food-related behavior in chronic obesity can be best framed within an Incentive Sensitization Theory. Implications of these findings for a brain-based therapy of obesity are briefly discussed.
AbstractList The dysregulation of food intake in chronic obesity has been explained by different theories. To assess their explanatory power, we meta-analyzed 22 brain-activation imaging studies. We found that obese individuals exhibit hyper-responsivity of the brain regions involved in taste and reward for food-related stimuli. Consistent with a Reward Surfeit Hypothesis, obese individuals exhibit a ventral striatum hyper-responsivity in response to pure tastes, particularly when fasting. Furthermore, we found that obese subjects display more frequent ventral striatal activation for visual food cues when satiated: this continued processing within the reward system, together with the aforementioned evidence, is compatible with the Incentive Sensitization Theory. On the other hand, we did not find univocal evidence in favor of a Reward Deficit Hypothesis nor for a systematic deficit of inhibitory cognitive control. We conclude that the available brain activation data on the dysregulated food intake and food-related behavior in chronic obesity can be best framed within an Incentive Sensitization Theory. Implications of these findings for a brain-based therapy of obesity are briefly discussed.The dysregulation of food intake in chronic obesity has been explained by different theories. To assess their explanatory power, we meta-analyzed 22 brain-activation imaging studies. We found that obese individuals exhibit hyper-responsivity of the brain regions involved in taste and reward for food-related stimuli. Consistent with a Reward Surfeit Hypothesis, obese individuals exhibit a ventral striatum hyper-responsivity in response to pure tastes, particularly when fasting. Furthermore, we found that obese subjects display more frequent ventral striatal activation for visual food cues when satiated: this continued processing within the reward system, together with the aforementioned evidence, is compatible with the Incentive Sensitization Theory. On the other hand, we did not find univocal evidence in favor of a Reward Deficit Hypothesis nor for a systematic deficit of inhibitory cognitive control. We conclude that the available brain activation data on the dysregulated food intake and food-related behavior in chronic obesity can be best framed within an Incentive Sensitization Theory. Implications of these findings for a brain-based therapy of obesity are briefly discussed.
•We provide the first quantitative assessment of neurocognitive theories of obesity.•These results were obtained with quantitative meta-analyses of fMRI studies.•Overall, we provide support for an incentive sensitization theory of obesity.•Obese individuals have greater activation of reward regions for visual food cues.•The brain of obese individuals is more sensitive to hunger and less to satiety. The dysregulation of food intake in chronic obesity has been explained by different theories. To assess their explanatory power, we meta-analyzed 22 brain-activation imaging studies. We found that obese individuals exhibit hyper-responsivity of the brain regions involved in taste and reward for food-related stimuli. Consistent with a Reward Surfeit Hypothesis, obese individuals exhibit a ventral striatum hyper-responsivity in response to pure tastes, particularly when fasting. Furthermore, we found that obese subjects display more frequent ventral striatal activation for visual food cues when satiated: this continued processing within the reward system, together with the aforementioned evidence, is compatible with the Incentive Sensitization Theory. On the other hand, we did not find univocal evidence in favor of a Reward Deficit Hypothesis nor for a systematic deficit of inhibitory cognitive control. We conclude that the available brain activation data on the dysregulated food intake and food-related behavior in chronic obesity can be best framed within an Incentive Sensitization Theory. Implications of these findings for a brain-based therapy of obesity are briefly discussed.
The dysregulation of food intake in chronic obesity has been explained by different theories. To assess their explanatory power, we meta-analyzed 22 brain-activation imaging studies. We found that obese individuals exhibit hyper-responsivity of the brain regions involved in taste and reward for food-related stimuli. Consistent with a Reward Surfeit Hypothesis, obese individuals exhibit a ventral striatum hyper-responsivity in response to pure tastes, particularly when fasting. Furthermore, we found that obese subjects display more frequent ventral striatal activation for visual food cues when satiated: this continued processing within the reward system, together with the aforementioned evidence, is compatible with the Incentive Sensitization Theory. On the other hand, we did not find univocal evidence in favor of a Reward Deficit Hypothesis nor for a systematic deficit of inhibitory cognitive control. We conclude that the available brain activation data on the dysregulated food intake and food-related behavior in chronic obesity can be best framed within an Incentive Sensitization Theory. Implications of these findings for a brain-based therapy of obesity are briefly discussed.
Author Devoto, F.
Bonandrini, R.
Luzi, L.
Banfi, G.
Zapparoli, L.
Paulesu, E.
Ferrulli, A.
Berlingeri, M.
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  orcidid: 0000-0002-3240-2341
  surname: Devoto
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  organization: fMRI Unit, IRCSS Istituto Ortopedico Galeazzi, Milan, Italy
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  surname: Bonandrini
  fullname: Bonandrini, R.
  organization: Department of Psychology and NeuroMi - Milan Centre for Neuroscience, University of Milano-Bicocca, Milan, Italy
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  orcidid: 0000-0002-3159-2809
  surname: Berlingeri
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  fullname: Luzi, L.
  organization: Endocrinology and Metabolic Diseases Unit, IRCCS Policlinico San Donato, San Donato Milanese, Milan, Italy
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  organization: fMRI Unit, IRCSS Istituto Ortopedico Galeazzi, Milan, Italy
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  surname: Paulesu
  fullname: Paulesu, E.
  email: eraldo.paulesu@unimib.it
  organization: fMRI Unit, IRCSS Istituto Ortopedico Galeazzi, Milan, Italy
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Mon Jul 21 05:59:15 EDT 2025
Thu Apr 24 23:11:11 EDT 2025
Tue Jul 01 01:19:37 EDT 2025
Fri Feb 23 02:23:13 EST 2024
IsDoiOpenAccess false
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Keywords CCA
Neuroimaging
OP
Obesity
VTA
Reward system
Activation likelihood estimation
CL
PFC
Hierarchical clustering
BP
HW
Meta-analysis
fMRI
OB
dlPFC
R-DVM
ALE
BOLD
HC
SN
PL
PET
BMI
Language English
License Copyright © 2018 Elsevier Ltd. All rights reserved.
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  text: November 2018
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PublicationTitle Neuroscience and biobehavioral reviews
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PublicationYear 2018
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Snippet •We provide the first quantitative assessment of neurocognitive theories of obesity.•These results were obtained with quantitative meta-analyses of fMRI...
The dysregulation of food intake in chronic obesity has been explained by different theories. To assess their explanatory power, we meta-analyzed 22...
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SubjectTerms Activation likelihood estimation
Animals
Appetite - physiology
Brain - diagnostic imaging
Brain - physiopathology
Food
Hierarchical clustering
Humans
Meta-analysis
Neuroimaging
Obesity
Obesity - diagnostic imaging
Obesity - physiopathology
Obesity - psychology
Perception - physiology
Reward system
Title Hungry brains: A meta-analytical review of brain activation imaging studies on food perception and appetite in obese individuals
URI https://dx.doi.org/10.1016/j.neubiorev.2018.07.017
https://www.ncbi.nlm.nih.gov/pubmed/30071209
https://www.proquest.com/docview/2083721406
Volume 94
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