Evidence map›Paper›PMID 23142231›Full record

ArticleGastroenterology2013

Developmental origins of functional dyspepsia-like gastric hypersensitivity in rats.

John H Winston, Sushil K Sarna

Open access · bronzeAbstract read
In one paragraph

Article in Gastroenterology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
3.3field-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

27 citing papers in PubMed, 47 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. Review
  7. Review
  8. Article
  9. Choosing an Animal Model for the Study of Functional Dyspepsia.Canadian journal of gastroenterology & hepatology · 2018
    Review
  10. Neonatal Colonic Inflammation: An Epigenetic Trigger of Adult Disease.Cellular and molecular gastroenterology and hepatology · 2018
    Article
  11. Article
  12. Article
  13. Article
  14. Gut Inflammation: More Than a Peripheral Annoyance.Digestive diseases and sciences · 2017
    Article
  15. Article
  16. Article
  17. Article
  18. Noninflammatory upregulation of nerve growth factor underlies gastric hypersensitivity induced by neonatal colon inflammation.American journal of physiology. Regulatory, integrative and comparative physiology · 2016
    Article
  19. Article
  20. 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

2 authors at 1 institution in 1 country.

John H WinstonEnteric Neuromuscular Disorders and Visceral Pain Center, Division of Gastroenterology, Department of Internal Medicine, The University of Texas Medical Branch at Galveston, Galveston, TX, USA.
Sushil K Sarna
The University of Texas Medical Branch at Galveston · US

Funding

Developmental Origins of Functional DyspepsiaR01DK088796 · NIDDK · UNIVERSITY OF TEXAS MED BR GALVESTON · PI SARNA, SUSHIL K · 2011 to 2014
$1.4M
NIDDK NIH HHS 5R01DK088796NIDDK NIH HHS R01 DK088796
6 · The paper itself

Abstract

BACKGROUND &

aimsGastric hypersensitivity (GHS) contributes to epigastric pain in patients with functional dyspepsia (FD); the etiology and cellular mechanisms of this dysfunction remain unknown. We investigated whether inflammatory insult to the colons of neonatal rats induced GHS in adult life.

methodsWe used cellular, molecular, and in vivo approaches to investigate the mechanisms of GHS in adult rats subjected to neonatal colonic insult by intraluminal administration of trinitrobenzene sulfonic acid; controls received saline. Six to 8 weeks later, rats were evaluated for GHS and tissue was collected for molecular experiments.

resultsInflammatory insult to the colon on post-natal day 10 caused an aberrant increase of corticosterone on post-natal day 15 and induced GHS in adult life. We called these FD-like rats. Inhibition of glucocorticoid receptors after neonatal insult blocked the induction of GHS in adult rats. The aberrant increase of plasma corticosterone in neonates increased the plasma concentration of norepinephrine, nerve growth factor in the gastric fundus muscularis externae, brain-derived neurotrophic factor in the thoracic dorsal root ganglia and spinal cord, and down-regulated K(v)1.1 messenger RNA in thoracic dorsal root ganglia without affecting the expression of K(v)1.4, Na(v)1.8, TrpA1, TrpV1, or P2X3 in FD-like rats. Inhibition of glucocorticoid receptors during neonatal insult or the inhibition of adrenergic receptors, nerve growth factor, or brain-derived neurotrophic factor in FD-like rats suppressed GHS. The intrathecal administration of small interfering RNAs against K(v)1.1 increased GHS in naive rats.

conclusionsInflammatory insult to the colons of rat pups leads to GHS in adult life. GHS is caused by altered expression of genes encoding neurotrophins and ion channels, and altered activity of the sympathetic nervous system.

Indexed as

Abdominal PainAnimalsColitisColonDisease Models, AnimalDyspepsiaGlucocorticoidsHypersensitivityMaleRatsRats, Sprague-DawleyReceptors, GlucocorticoidStomach DiseasesTrinitrobenzenesulfonic AcidGlucocorticoidsReceptors, GlucocorticoidTrinitrobenzenesulfonic Acid

Identifiers

PMID23142231
PMCPMC3578170
OpenAlexW1976845967

What OpenQuestion holds

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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.