Evidence map›Paper›PMID 23897220›Full record

ArticleInternational journal of obesity (2005)2014

Altered gastric vagal mechanosensitivity in diet-induced obesity persists on return to normal chow and is accompanied by increased food intake.

S J Kentish, T A O'Donnell, C L Frisby, H Li, G A Wittert, A J Page

Abstract read
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In one paragraph

Article in International journal of obesity (2005), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
2.6field-weighted citation impact, top 12% 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

26 citing papers in PubMed, 48 citations in OpenAlex.

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  13. The metabolic role of vagal afferent innervation.Nature reviews. Gastroenterology & hepatology · 2018
    Review
  14. The vagus neurometabolic interface and clinical disease.International journal of obesity (2005) · 2018
    Review
  15. Review
  16. Review
  17. High-Fat Diet-Induced Obesity Ablates Gastric Vagal Afferent Circadian Rhythms.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016
    Article
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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

6 authors at 2 institutions in 1 country.

S J KentishNerve-Gut Research Laboratory, Hanson Institute, Discipline of Medicine, University of Adelaide, Adelaide, SA, Australia.
T A O'DonnellRoyal Adelaide Hospital, Adelaide, SA, Australia.
C L FrisbyRoyal Adelaide Hospital, Adelaide, SA, Australia.
H LiNerve-Gut Research Laboratory, Hanson Institute, Discipline of Medicine, University of Adelaide, Adelaide, SA, Australia.
G A WittertNerve-Gut Research Laboratory, Hanson Institute, Discipline of Medicine, University of Adelaide, Adelaide, SA, Australia.
A J Page1] Nerve-Gut Research Laboratory, Hanson Institute, Discipline of Medicine, University of Adelaide, Adelaide, SA, Australia [2] Royal Adelaide Hospital, Adelaide, SA, Australia.
Royal Adelaide Hospital · AUUniversity of Adelaide · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND AND

aimsGastric vagal afferents convey satiety signals in response to mechanical stimuli. The sensitivity of these afferents is decreased in diet-induced obesity. Leptin, secreted from gastric epithelial cells, potentiates the response of vagal afferents to mechanical stimuli in lean mice, but has an inhibitory effect in high-fat diet (HFD)-induced obese mice. We sought to determine whether changes in vagal afferent function and response to leptin in obesity were reversible by returning obese mice consuming a HFD to standard laboratory chow diet (SLD).

methodsEight-week-old female C57BL/6 mice were either fed a SLD (N=20) or HFD (N=20) for 24 weeks. A third group was fed a HFD for 12 weeks and then a SLD for a further 12 weeks (RFD, N=18). An in vitro gastro-oesophageal vagal afferent preparation was used to determine the mechanosensitivity of gastric vagal afferents and the modulatory effect of leptin (0.1-10 nM) was examined. Retrograde tracing and quantitative RT-PCR were used to determine the expression of leptin receptor (LepR) messenger RNA (mRNA) in whole nodose and specific cell bodies traced from the stomach.

resultsAfter 24 weeks, both the HFD and RFD mice had increased body weight, gonadal fat mass, plasma leptin, plasma insulin and daily energy consumption compared with the SLD mice. The HFD and RFD mice had reduced tension receptor mechanosensitivity and leptin further inhibited responses to tension in HFD, RFD but not SLD mice. Mucosal receptors from both the SLD and RFD mice were potentiated by leptin, an effect not seen in HFD mice. LepR expression was unchanged in the whole nodose, but was reduced in the mucosal afferents of the HFD and RFD mice.

conclusionDisruption of gastric vagal afferent function by HFD-induced obesity is only partially reversible by dietary change, which provides a potential mechanism preventing maintenance of weight loss.

Indexed as

Afferent PathwaysAnimalsBody WeightDiet, High-FatEnergy IntakeFeeding BehaviorFemaleGastric MucosaImmunohistochemistryLeptinMiceMice, Inbred C57BLObesityReal-Time Polymerase Chain ReactionReceptors, LeptinThinnessLeptinReceptors, Leptin

Identifiers

PMID23897220
OpenAlexW2003224159

What OpenQuestion holds

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Read underepoch 390

Registered trials

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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.