Cited by 64Regulation of Appetite and ObesityEating Disorders and BehaviorsNeurotransmitter Receptor Influence on Behavior

Association of Body Mass and Brain Activation during Gastric Distention: Implications for Obesity

Open access
Tomasi, Dardo, Wang, Gene-Jack, Wang, Ruiliang, Backus, Walter, Geliebter, Allan, Telang, Frank, Jayne, Millar C., Wong, Christopher +2 more·2009·PLoS ONE

Abstract

BACKGROUND: Gastric distention (GD), as it occurs during meal ingestion, signals a full stomach and it is one of the key mechanisms controlling food intake. Previous studies on GD showed lower activation of the amygdala for subjects with higher body mass index (BMI). Since obese subjects have dopaminergic deficits that correlate negatively with BMI and the amygdala is innervated by dopamine neurons, we hypothesized that BMI would correlate negatively with activation not just in the amygdala but also in other dopaminergic brain regions (midbrain and hypothalamus). METHODOLOGY/PRINCIPAL FINDINGS: We used functional magnetic resonance imaging (fMRI) to evaluate brain activation during GD in 24 healthy subjects with BMI range of 20-39 kg/m(2). Using multiple regression and cross-correlation analyses based on a family-wise error corrected threshold P = 0.05, we show that during slow GD to maximum volumes of 500 ml and 700 ml subjects with increased BMI had increased activation in cerebellum and left posterior insula, and decreased activation of dopaminergic (amygdala, midbrain, hypothalamus, thalamus) and serotonergic (pons) brain regions and anterior insula, regions that were functionally interconnected with one another. CONCLUSIONS: The negative correlation between BMI and BOLD responses to gastric distention in dopaminergic (midbrain, hypothalamus, amygdala, thalamus) and serotonergic (pons) brain regions is consistent with disruption of dopaminergic and serotonergic signaling in obesity. In contrast the positive correlation between BMI and BOLD responses in posterior insula and cerebellum suggests an opposing mechanism that promotes food intake in obese subjects that may underlie their ability to consume at once large food volumes despite increasing gastric distention.

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Integrity signals

Registry

Crossref · 10.1371/journal.pone.0006847

Cites

76 of 76 references verified0 citation errors · 0 not checkable

Statistics

Claims the paper makes

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

  • In lean but not obese subjects, gastric distension resulted in activation of the amygdala and deactivation of the anterior insula.

    “Moreover, in lean, but not in obese subjects, gastric distension resulted in activation of the amygdala and deactivation of the anterior insula (141).”

    From Obesity and addiction: Neurobiological overlaps (2013) · cites this paper as [141]

  • In lean but not obese subjects, gastric distention activated the amygdala and deactivated the anterior insula.

    “Moreover, in lean but not in obese subjects, gastric distention resulted in activation of the amygdala and deactivation of the anterior insula (100).”

    From The Addictive Dimensionality of Obesity (2013) · cites this paper as [100]

  • In lean but not in obese subjects, gastric distention resulted in activation of the amygdala and deactivation of the anterior insula.

    “Moreover, in lean but not in obese subjects gastric distention resulted in activation of the amygdala and deactivation of the anterior insula (Tomasi et al 2009).”

    From Food and Drug Reward: Overlapping Circuits in Human Obesity and Addiction (2011) · cites this paper as Tomasi et al 2009

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

The self-check needs the paper’s full text.

Cites

Flagged first, then by citations

Research works printed but not linked: 1

  1. [29]Balcioglu A Wurtman R 1998 International Journal of Obesity and Related Metabolic Disorders 22 325 328 9578237

Cited by

Sorted by citations

Authors
Tomasi, D., Wang, G.-J., Wang, R., Backus, W., Geliebter, A., Telang, F., Jayne, M. C., Wong, C., Fowler, J. S., & Volkow, N. D.
Affiliations
  • National Institutes of Health (US)
  • Brookhaven National Laboratory (US)
  • Stony Brook University (US)
  • Columbia University (US)
Corresponding author
Tomasi, Dardo
Venue
PLoS ONE
Published
2009-08-31
Volume
4
Issue
8
Pages
e6847
ISSN
1932-6203 (ISSN-L)
OpenAlex
W2022546100
Cited by
64
References
76
Citations by year
2026: 4 · 2025: 3 · 2024: 2 · 2022: 2 · 2021: 3 · 2020: 3 · 2019: 2 · 2018: 6 · 2017: 2 · 2016: 3 · 2015: 9 · 2014: 1 · 2013: 6 · 2012: 6
FWCI
2.69
Type
journal article
Language
en
Open access
Locations
  • PLoS ONE (publishedVersion, public-domain)
  • PubMed Central (publishedVersion, public-domain)
  • PubMed (publishedVersion)
  • OSTI OAI (U.S. Department of Energy Office of Scientific and Technical Information) (submittedVersion)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
Funders
  • U.S. Department of Energy
  • Deutsches Krebsforschungszentrum
  • National Institute on Alcohol Abuse and Alcoholism (Y1 AA 3009, R01AA009481, R01AA09481)
  • National Institute on Drug Abuse (R01DA006278, R01DA006891)
  • National Institute of Diabetes and Digestive and Kidney Diseases (R56DK080153, R01DK054318, R01DK080153)
  • National Center for Research Resources (#M01RR10710, M01RR010710, 5M01-RR-10710, RR-10710, M01-RR)
  • Biological and Environmental Research
  • Brookhaven National Laboratory
Topics
  • Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Regulation of Appetite and Obesity
  • Social Sciences › Psychology › Clinical Psychology › Eating Disorders and Behaviors
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
Keywords
gastric distension, body mass index, obesity, food intake regulation, amygdala, midbrain, hypothalamus, thalamus, dopaminergic signaling, serotonergic signaling, posterior insula, cerebellum, BOLD signal, meal ingestion
MeSH terms
Adult, Body Weight, Brain, Energy Intake, Female, Humans, Magnetic Resonance Imaging, Male, Obesity, Stomach

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review