Evidence map›Paper›PMID 25496312›Full record

ArticleBMC gastroenterology2014

Structural and functional consequences of buserelin-induced enteric neuropathy in rat.

Elin Sand, Bodil Roth, Björn Weström, Peter Bonn, Eva Ekblad, Bodil Ohlsson

Open access · goldAbstract read
In one paragraph

Article in BMC gastroenterology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.8field-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

9 citing papers in PubMed, 13 citations in OpenAlex.

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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 3 institutions in 1 country.

Elin SandDepartment of Clinical Sciences, Division of Internal Medicine Skåne University Hospital, Lund University, Inga Marie Nilssons street 32, S-205 02, Malmö, Sweden. elin.sand@med.lu.se.
Bodil RothDepartment of Clinical Sciences, Division of Internal Medicine Skåne University Hospital, Lund University, Inga Marie Nilssons street 32, S-205 02, Malmö, Sweden. bodil.roth@med.lu.se.
Björn WeströmDepartment of Biology, Functional Biology, Lund University, 221 00, Lund, Sweden. bjorn.westrom@biol.lu.se.
Peter BonnDepartment of Medicinal Chemistry, CVMD, AstraZeneca, Mölndal, Sweden. peter.g.bonn@gmail.com.
Eva EkbladDepartment of Experimental Medical Science, Neurogastroenterology Unit, BMC B11, Lund University, 221 84, Lund, Sweden. eva.ekblad@med.lu.se.
Bodil OhlssonDepartment of Clinical Sciences, Division of Internal Medicine Skåne University Hospital, Lund University, Inga Marie Nilssons street 32, S-205 02, Malmö, Sweden. bodil.ohlsson@med.lu.se.
Lund University · SEAstraZeneca (Sweden) · SESkåne University Hospital · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundWomen treated with gonadotropin-releasing hormone (GnRH) analogs may develop enteric neuropathy and dysmotility. Administration of a GnRH analog to rats leads to similar degenerative neuropathy and ganglioneuritis. The aim of this study on rat was to evaluate the early GnRH-induced enteric neuropathy in terms of distribution of neuronal subpopulations and gastrointestinal (GI) function.

methodsForty rats were given the GnRH analog buserelin (20 μg, 1 mg/ml) or saline subcutaneously, once daily for 5 days, followed by 3 weeks of recovery, representing one treatment session. Two weeks after the fourth treatment session, the animals were tested for GI transit time and galactose absorption, and fecal weight and fat content was analyzed. After sacrifice, enteric neuronal subpopulations were analyzed. Blood samples were analyzed for zonulin and antibodies against GnRH and luteinizing hormone, and their receptors.

resultsBuserelin treatment transiently increased the body weight after 5 and 9 weeks (p < 0.001). Increased estradiol in plasma and thickened uterine muscle layers indicate high estrogen activity. The numbers of both submucous and myenteric neurons were reduced by 27%-61% in ileum and colon. The relative numbers of neurons containing calcitonin gene-related peptide (CGRP), cocaine- and amphetamine-related transcript (CART), galanin, gastrin-releasing peptide (GRP), neuropeptide Y (NPY), nitric oxide synthase (NOS), serotonin, substance P (SP), vasoactive intestinal peptide (VIP) or vesicular acetylcholine transporter (VAchT), and their nerve fiber density, were unchanged after buserelin treatment, but the relative number of submucous neurons containing somatostatin tended to be increased (p = 0.062). The feces weight decreased in buserelin-treated rats (p < 0.01), whereas feces fat content increased (p < 0.05), compared to control rats. Total GI transit time, galactose absorption, zonulin levels in plasma, and antibody titers in serum were unaffected by buserelin treatment.

conclusionsA marked enteric neuronal loss with modest effects on GI function is found after buserelin treatment. Increased feces fat content is suggested an early sign of dysfunction.

Indexed as

AnimalsBuserelinColonDisease Models, AnimalEstradiolFecesFemaleGastrointestinal TractGastrointestinal TransitIleumIntestinal Pseudo-ObstructionLipidsNeuronsRats, Sprague-DawleyStomachUterusBuserelinEstradiolLipids

Identifiers

PMID25496312
PMCPMC4275936
OpenAlexW2091880667

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.