Evidence map›Paper›PMID 25840667›Full record

ArticleEuropean journal of nutrition2016

Adaptive response activated by dietary cis9, trans11 conjugated linoleic acid prevents distinct signs of gliadin-induced enteropathy in mice.

Paolo Bergamo, Gianna Palmieri, Ennio Cocca, Ida Ferrandino, Marta Gogliettino, Antonio Monaco, Francesco Maurano, Mauro Rossi

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Article in European journal of nutrition, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
0.9field-weighted citation impact, top 25% 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

10 citing papers in PubMed, 17 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

8 authors at 3 institutions in 1 country.

Paolo BergamoInstitute of Food Sciences, National Research Council (CNR-ISA), Via Roma 64, 83100, Avellino, Italy. p.bergamo@isa.cnr.it.
Gianna PalmieriInstitute of Biosciences and Bioresources, National Research Council (CNR-IBBR), Naples, Italy.
Ennio CoccaInstitute of Biosciences and Bioresources, National Research Council (CNR-IBBR), Naples, Italy.
Ida FerrandinoDepartment of Biology, University "Federico II" of Naples, Naples, Italy.
Marta GogliettinoInstitute of Biosciences and Bioresources, National Research Council (CNR-IBBR), Naples, Italy.
Antonio MonacoDepartment of Biology, University "Federico II" of Naples, Naples, Italy.
Francesco MauranoInstitute of Food Sciences, National Research Council (CNR-ISA), Via Roma 64, 83100, Avellino, Italy.
Mauro RossiInstitute of Food Sciences, National Research Council (CNR-ISA), Via Roma 64, 83100, Avellino, Italy.
National Research Council · ITUniversity of Naples Federico II · ITInstitute of Food Science · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeThe beneficial effects of conjugated linoleic acid (CLA) mixture (cis9, trans11, c9; trans10, cis12, t10) against gliadin-induced toxicity in HLA-DQ8-transgenic mice (DQ8) have been associated with improved duodenal cytoprotective mechanisms [nuclear factor-E2-related factor-2, Nrf2; acylpeptide hydrolase (APEH)/proteasome]. The present study was aimed at investigating the ability of individual CLA isomers to improve the efficacy of these defensive mechanisms and to protect against duodenal injury caused by the combined administration of gliadin and indomethacin (GI).

methodsGluten-mediated enteropathy was induced in DQ8 mice by three intra-gastric administration of gliadin (20 mg kg(-1)/bw) and indomethacin (15 mg L(-1)) in drinking water for 10 days (GI). C9 or t10 CLA (520 mg kg(-1)/bw/day) were orally administered for 2 weeks. Pro-oxidant and toxic effects associated with GI treatment, anti-oxidant/detoxifying ability of c9 or t10-CLA and the protective effect induced by c9 pre-treatment (c9 + GI) were evaluated in DQ8 mice duodenum by combining enzymatic, immunoblotting, histological evaluation and quantitative real-time PCR assays.

resultsGI treatment produces the time-dependent decline of the considered detoxifying mechanisms thus leading to pro-apoptotic and pro-oxidant effects. APEH/proteasome pathway was not markedly affected by individual CLA isomers, but duodenal redox status and activity/mRNA levels of Nrf2-activated enzymes were significantly improved by c9 administration. c9 pre-treatment protects against GI-mediated accumulation of oxidative stress markers, and histological examination reveals the increase of goblet cells number in mouse duodenum but induces only a partial recovery of APEH/proteasome activity.

conclusionsThe activation of and adaptive response by low doses of c9 supplementation prevents distinct signs of gliadin-induced enteropathy in DQ8 mice.

Indexed as

AnimalsCeliac DiseaseDose-Response Relationship, DrugGliadinIndomethacinLinoleic Acids, ConjugatedMiceMice, TransgenicNAD(P)H Dehydrogenase (Quinone)NF-E2-Related Factor 2Oxidative StressPeptide HydrolasesReactive Oxygen Speciesacylaminoacyl-peptidasecis-9, trans-11-conjugated linoleic acidGliadinIndomethacinLinoleic Acids, ConjugatedNAD(P)H Dehydrogenase (Quinone)Nfe2l2 protein, mouseNF-E2-Related Factor 2Nqo1 protein, mousePeptide HydrolasesReactive Oxygen SpeciesAdaptive responseCeliac diseaseConjugated linoleic acidFatty acidsGliadinNrf2

Identifiers

PMID25840667
OpenAlexW2010382608

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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.