Evidence map›Paper›PMID 23266933›Full record

ArticleThe Journal of physiology2013

Gastric vagal afferent modulation by leptin is influenced by food intake status.

Stephen J Kentish, Tracey A O'Donnell, Nicole J Isaacs, Richard L Young, Hui Li, Andrea M Harrington, Stuart M Brierley, Gary A Wittert, L Ashley Blackshaw, Amanda J Page

Open access · greenAbstract read
In one paragraph

Article in The Journal of physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
2.9field-weighted citation impact, top 9% 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

42 citing papers in PubMed, 90 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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  17. Stress-induced modulation of vagal afferents.Neurogastroenterology and motility · 2019
    Review
  18. Article
  19. Article
  20. The metabolic role of vagal afferent innervation.Nature reviews. Gastroenterology & hepatology · 2018
    Review
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

10 authors at 3 institutions in 2 countries.

Stephen J KentishNerve-Gut Research Laboratory, Room 1-216-H, Level 1, Hanson Institute, Royal Adelaide Hospital, Adelaide, SA 5000, Australia.
Tracey A O'Donnell
Nicole J Isaacs
Richard L Young
Hui Li
Andrea M Harrington
Stuart M Brierley
Gary A Wittert
L Ashley Blackshaw
Amanda J Page
Hanson Institute · AURoyal Adelaide Hospital · AUQueen Mary University of London · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Energy intake is strongly influenced by vagal afferent signals from the stomach, and is also modulated by leptin. Leptin may be secreted from gastric epithelial cells, so we aimed to determine the direct effect of leptin on gastric vagal afferents under different feeding conditions. Female C57BL/6 mice were fed standard laboratory diet, high-fat diet or were food restricted. The expression of leptin receptor (Lep-R) and its signal transduction molecules in vagal afferents was determined by retrograde tracing and reverse-transcription polymerase chain reaction, and the relationship between leptin-immunopositive cells and gastric vagal afferent endings determined by anterograde tracing and leptin immunohistochemistry. An in vitro preparation was used to determine the functional effects of leptin on gastric vagal afferents and the second messenger pathways involved. Leptin potentiated vagal mucosal afferent responses to tactile stimuli, and epithelial cells expressing leptin were found close to vagal mucosal endings. After fasting or diet-induced obesity, potentiation of mucosal afferents by leptin was lost and Lep-R expression reduced in the cell bodies of gastric mucosal afferents. These effects in diet-induced obese mice were accompanied by a reduction in anatomical vagal innervation of the gastric mucosa. In striking contrast, after fasting or diet-induced obesity, leptin actually inhibited responses to distension in tension receptors. The inhibitory effect on gastric tension receptors was mediated through phosphatidylinositol 3-kinase-dependent activation of large-conductance calcium-activated potassium channels. The excitatory effect of leptin on gastric mucosal vagal afferents was mediated by phospholipase C-dependent activation of canonical transient receptor potential channels. These data suggest the effect of leptin on gastric vagal afferent excitability is dynamic and related to the feeding state. Paradoxically, in obesity, leptin may reduce responses to gastric distension following food intake.

Indexed as

AnimalsDiet, High-FatEatingFemaleGastric MucosaLeptinMiceMice, Inbred C57BLMuscle, SmoothNodose GanglionObesityReceptors, LeptinVagus NerveLeptinReceptors, Leptin

Identifiers

PMID23266933
PMCPMC3624860
OpenAlexW1542237172

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.