Evidence map›Paper›PMID 28545056›Full record

ArticlePloS one2017

Effect of Helicobacter pylori infection on the link between GLP-1 expression and motility of the gastrointestinal tract.

Hirotsugu Eda, Hirokazu Fukui, Ryosuke Uchiyama, Yoshitaka Kitayama, Ken Hara, Mo Yang, Mio Kodani, Toshihiko Tomita, Tadayuki Oshima, Jiro Watari and 2 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

4 citing papers in PubMed, 10 citations in OpenAlex.

  1. Observational
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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

12 authors at 1 institution in 2 countries.

Hirotsugu EdaDivision of Gastroenterology, Department of Internal Medicine, Hyogo College of Medicine, Nishinomiya, Japan.
Hirokazu FukuiDivision of Gastroenterology, Department of Internal Medicine, Hyogo College of Medicine, Nishinomiya, Japan.ORCID http://orcid.org/0000-0002-8642-5784
Ryosuke UchiyamaDepartment of Microbiology, Hyogo College of Medicine, Nishinomiya, Japan.
Yoshitaka KitayamaDivision of Gastroenterology, Department of Internal Medicine, Hyogo College of Medicine, Nishinomiya, Japan.
Ken HaraDivision of Gastroenterology, Department of Internal Medicine, Hyogo College of Medicine, Nishinomiya, Japan.
Mo YangDivision of Gastroenterology, Department of Internal Medicine, Hyogo College of Medicine, Nishinomiya, Japan.
Mio KodaniDivision of Gastroenterology, Department of Internal Medicine, Hyogo College of Medicine, Nishinomiya, Japan.
Toshihiko TomitaDivision of Gastroenterology, Department of Internal Medicine, Hyogo College of Medicine, Nishinomiya, Japan.
Tadayuki OshimaDivision of Gastroenterology, Department of Internal Medicine, Hyogo College of Medicine, Nishinomiya, Japan.
Jiro WatariDivision of Gastroenterology, Department of Internal Medicine, Hyogo College of Medicine, Nishinomiya, Japan.
Hiroko TsutsuiDepartment of Microbiology, Hyogo College of Medicine, Nishinomiya, Japan.
Hiroto MiwaDivision of Gastroenterology, Department of Internal Medicine, Hyogo College of Medicine, Nishinomiya, Japan.
Hyogo Medical University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAlthough Helicobacter pylori (H. pylori) infection is closely associated with the development of peptic ulcer, its involvement in pathophysiology in the lower intestinal tract and gastrointestinal (GI) motility remains unclear. Glucagon-like peptide-1 (GLP-1) is a gut hormone produced in the lower intestinal tract and involved in GI motility. Here, we investigated the effect of H. pylori infection on the link between GLP-1 expression and motility of the GI tract.

methodsC57BL/6 mice were inoculated with a H. pylori strain. Twelve weeks later, the H. pylori-infected mice underwent H. pylori eradication treatment. GI tissues were obtained from the mice at various time intervals, and evaluated for the severity of gastric inflammatory cell infiltration and immunohistochemical expression of GLP-1 and PAX6 in the colonic mucosa. Gastrointestinal transit time (GITT) was measured by administration of carmine-red solution.

resultsGLP-1 was expressed in the endocrine cells of the colonic mucosa, and PAX6 immunoreactivity was co-localized in such cells. The numbers of GLP-1- and PAX6-positive cells in the colon were significantly increased at 12 weeks after H. pylori infection and showed a positive correlation with each other. The GITT was significantly longer in H. pylori-infected mice than in non-infected controls and showed a positive correlation with GLP-1 expression. When H. pylori-infected mice underwent H. pylori eradication, GITT and PAX6/GLP-1 expression did not differ significantly from those in untreated H. pylori-infected mice.

conclusionsH. pylori infection may impair GI motility by enhancing the colonic GLP-1/PAX6 expression.

Indexed as

AnimalsColonFemaleGastrointestinal MotilityGlucagon-Like Peptide 1Helicobacter InfectionsHelicobacter pyloriMice, Inbred C57BLPAX6 Transcription FactorGlucagon-Like Peptide 1Pax6 protein, mousePAX6 Transcription Factor

Identifiers

PMID28545056
PMCPMC5436696
OpenAlexW2615739552

What OpenQuestion holds

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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.