Evidence map›Paper›PMID 29456586›Full record

ArticleNutrition & metabolism2018

Dietary canolol protects the heart against the deleterious effects induced by the association of rapeseed oil, vitamin E and coenzyme Q10 in the context of a high-fat diet.

Thibault Leger, Isabelle Hininger-Favier, Frédéric Capel, Alain Geloen, Jean-Paul Rigaudière, Chrystèle Jouve, Elodie Pitois, Gaelle Pineau, Carole Vaysse, Jean-Michel Chardigny and 3 more

Open access · goldAbstract read
In one paragraph

Article in Nutrition & metabolism, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
1.6field-weighted citation impact, top 17% 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

6 citing papers in PubMed, 23 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

13 authors at 5 institutions in 1 country.

Thibault LegerUniversité Clermont Auvergne, INRA, UNH, Unité de Nutrition Humaine, CRNH Auvergne, 58 rue Montalembert, BP 321, 63009 Clermont-Ferrand cedex 1, France.
Isabelle Hininger-Favier2Univ. Grenoble Alpes, INSERM, LBFA, 38000 Grenoble, France.
Frédéric CapelUniversité Clermont Auvergne, INRA, UNH, Unité de Nutrition Humaine, CRNH Auvergne, 58 rue Montalembert, BP 321, 63009 Clermont-Ferrand cedex 1, France.
Alain Geloen3Univ-Lyon, laboratoire CarMeN, INRA UMR1397, INSERM U1060, Université Claude Bernard Lyon 1, INSA-Lyon, IMBL, 69621 Villeurbanne, France.
Jean-Paul RigaudièreUniversité Clermont Auvergne, INRA, UNH, Unité de Nutrition Humaine, CRNH Auvergne, 58 rue Montalembert, BP 321, 63009 Clermont-Ferrand cedex 1, France.
Chrystèle JouveUniversité Clermont Auvergne, INRA, UNH, Unité de Nutrition Humaine, CRNH Auvergne, 58 rue Montalembert, BP 321, 63009 Clermont-Ferrand cedex 1, France.
Elodie PitoisUniversité Clermont Auvergne, INRA, UNH, Unité de Nutrition Humaine, CRNH Auvergne, 58 rue Montalembert, BP 321, 63009 Clermont-Ferrand cedex 1, France.
Gaelle Pineau3Univ-Lyon, laboratoire CarMeN, INRA UMR1397, INSERM U1060, Université Claude Bernard Lyon 1, INSA-Lyon, IMBL, 69621 Villeurbanne, France.
Carole Vaysse4ITERG-ENMS, Université de Bordeaux, rue Léo Saignat, 33076 Bordeaux cedex, France.
Jean-Michel ChardignyUniversité Clermont Auvergne, INRA, UNH, Unité de Nutrition Humaine, CRNH Auvergne, 58 rue Montalembert, BP 321, 63009 Clermont-Ferrand cedex 1, France.
Marie-Caroline Michalski3Univ-Lyon, laboratoire CarMeN, INRA UMR1397, INSERM U1060, Université Claude Bernard Lyon 1, INSA-Lyon, IMBL, 69621 Villeurbanne, France.
Corinne Malpuech-BrugèreUniversité Clermont Auvergne, INRA, UNH, Unité de Nutrition Humaine, CRNH Auvergne, 58 rue Montalembert, BP 321, 63009 Clermont-Ferrand cedex 1, France.
Luc DemaisonUniversité Clermont Auvergne, INRA, UNH, Unité de Nutrition Humaine, CRNH Auvergne, 58 rue Montalembert, BP 321, 63009 Clermont-Ferrand cedex 1, France.ORCID 0000-0003-0771-7250
Unité de Nutrition Humaine · FRUniversité Claude Bernard Lyon 1 · FRInserm · FRInstitut Agro Dijon · FRUniversité de Bordeaux · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundObesity progressively leads to cardiac failure. Omega-3 polyunsaturated fatty acids (PUFA) have been shown to have cardio-protective effects in numerous pathological situations. It is not known whether rapeseed oil, which contains α-linolenic acid (ALA), has a similar protective effect. Omega-3 PUFAs are sensitive to attack by reactive oxygen species (ROS), and lipid peroxidation products could damage cardiac cells. We thus tested whether dietary refined rapeseed oil (RSO) associated with or without different antioxidants (vitamin E, coenzyme Q10 and canolol) is cardio-protective in a situation of abdominal obesity.

methodsSixty male Wistar rats were subdivided into 5 groups. Each group was fed a specific diet for 11 weeks: a low-fat diet (3% of lipids, C diet) with compositionally-balanced PUFAs; a high-fat diet rich in palm oil (30% of lipids, PS diet); the PS diet in which 40% of lipids were replaced by RSO (R diet); the R diet supplemented with coenzyme Q10 (CoQ10) and vitamin E (RTC diet); and the RTC diet supplemented with canolol (RTCC diet). At the end of the diet period, the rats were sacrificed and the heart was collected and immediately frozen. Fatty acid composition of cardiac phospholipids was then determined. Several features of cardiac function (fibrosis, inflammation, oxidative stress, apoptosis, metabolism, mitochondrial biogenesis) were also estimated.

resultsAbdominal obesity reduced cardiac oxidative stress and apoptosis rate by increasing the proportion of arachidonic acid (AA) in membrane phospholipids. Dietary RSO had the same effect, though it normalized the proportion of AA. Adding vitamin E and CoQ10 in the RSO-rich high fat diet had a deleterious effect, increasing fibrosis by increasing angiotensin-2 receptor-1b (Ag2R-1b) mRNA expression. Overexpression of these receptors triggers coronary vasoconstriction, which probably induced ischemia. Canolol supplementation counteracted this deleterious effect by reducing coronary vasoconstriction.

conclusionCanolol was found to counteract the fibrotic effects of vitamin E + CoQ10 on cardiac fibrosis in the context of a high-fat diet enriched with RSO. This effect occurred through a restoration of cardiac Ag2R-1b mRNA expression and decreased ischemia.

Indexed as

AntioxidantCanololHeartObesityRapeseed oilω3 PUFAs

Identifiers

PMID29456586
PMCPMC5809903
OpenAlexW2788587390

What Socratic holds

Textmetadata
LicenceCC BY
Read underepoch 390

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 Socratic graph.