Evidence map›Paper›PMID 21486762›Full record

ArticleThe Journal of physiology2011

Impaired intestinal afferent nerve satiety signalling and vagal afferent excitability in diet induced obesity in the mouse.

Donna M Daly, Sung Jin Park, William C Valinsky, Michael J Beyak

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of physiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 114 papers.

0numbers the graph read from it
0cells of the map it votes in
114citing papers in PubMed
5.4field-weighted citation impact, top 3% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

114 citing papers in PubMed, 184 citations in OpenAlex.

  1. Trial
  2. The critical role of gut-brain signalling in eating behaviour and obesity.Nature reviews. Gastroenterology & hepatology · 2026
    Review
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  5. Article
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  8. In autonomic adaptation the details matter.The Journal of physiology · 2026
    Article
  9. Article
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  11. Article
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  15. Microbiome: A Key Regulator of Body-Brain Interactions.Advances in experimental medicine and biology · 2025
    Review
  16. Review
  17. Review
  18. Review
  19. Article
  20. Cholinergic Neurotransmission Controls Orexigenic Endocannabinoid Signaling in the Gut in Diet-Induced Obesity.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024
    Article

54 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 2 institutions in 1 country.

Donna M DalyDepartments of Medicine and Physiology, Gastrointestinal Diseases Research Unit (GIDRU) Wing, Kingston General Hospital, 76 Stuart Street, Kingston, Ontario, Canada K7L2V7.
Sung Jin Park
William C Valinsky
Michael J Beyak
Queen's University · CAKingston General Hospital · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Gastrointestinal vagal afferents transmit satiety signals to the brain via both chemical and mechanical mechanisms. There is indirect evidence that these signals may be attenuated in obesity. We hypothesized that responses to satiety mediators and distension of the gut would be attenuated after induction of diet induced obesity. Obesity was induced by feeding a high fat diet (60% kcal from fat). Low fat fed mice (10% kcal from fat) served as a control. High fat fed mice were obese, with increased visceral fat, but were not hyperglycaemic. Recordings from jejunal afferents demonstrated attenuated responses to the satiety mediators cholecystokinin (CCK, 100 nm) and 5-hydroxytryptamine (5-HT, 10 μm), as was the response to low intensity jejunal distension, while responses to higher distension pressures were preserved. We performed whole cell patch clamp recordings on nodose ganglion neurons, both unlabelled, and those labelled by fast blue injection into the wall of the jejunum. The cell membrane of both labelled and unlabelled nodose ganglion neurons was less excitable in HFF mice, with an elevated rheobase and decreased number of action potentials at twice rheobase. Input resistance of HFF neurons was also significantly decreased. Calcium imaging experiments revealed reduced proportion of nodose ganglion neurons responding to CCK and 5-HT in obese mice. These results demonstrate a marked reduction in afferent sensitivity to satiety related stimuli after a chronic high fat diet. A major mechanism underlying this change is reduced excitability of the neuronal cell membrane. This may explain the development of hyperphagia when a high fat diet is consumed. Improving sensitivity of gastrointestinal afferent nerves may prove useful to limit food intake in obesity.

Indexed as

Action PotentialsAfferent PathwaysAnimalsBlood GlucoseBody WeightCalcium SignalingCholecystokininDietary FatsElectric ImpedanceIntestinesIntra-Abdominal FatJejunumMaleMechanotransduction, CellularMembrane PotentialsMiceBlood GlucoseCholecystokininDietary FatsSerotonin

Identifiers

PMID21486762
PMCPMC3112560
OpenAlexW2130705536

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.