Evidence map›Paper›PMID 36778746›Full record

ArticleFunction (Oxford, England)2023

Comparing Transgenic Production to Supplementation of ω-3 PUFA Reveals Distinct But Overlapping Mechanisms Underlying Protection Against Metabolic and Hepatic Disorders.

Noëmie Daniel, Mélanie Le Barz, Patricia L Mitchell, Thibault V Varin, Isabelle Bourdeau Julien, Dominique Farabos, Geneviève Pilon, Josée Gauthier, Carole Garofalo, Jing X Kang and 12 more

Open access · goldAbstract read
In one paragraph

Article in Function (Oxford, England), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed, 1 pooled it
1.4field-weighted citation impact, top 21% 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

11 citing papers in PubMed, 1 synthesis or guideline pooled it, 12 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

22 authors at 6 institutions in 3 countries.

Noëmie DanielFaculty of Agricultural and Food Sciences, School of Nutrition, Laval University, Quebec, QC G1V 0A6, Canada.
Mélanie Le BarzQuebec Heart and Lung Institute Research Centre, Laval University, Quebec, QC G1V 4G5, Canada.
Patricia L MitchellQuebec Heart and Lung Institute Research Centre, Laval University, Quebec, QC G1V 4G5, Canada.
Thibault V VarinQuebec Heart and Lung Institute Research Centre, Laval University, Quebec, QC G1V 4G5, Canada.
Isabelle Bourdeau JulienInstitute of Nutrition and Functional Foods (INAF), Centre NUTRISS, Quebec, QC G1V 0A6, Canada.
Dominique FarabosSaint Antoine Research Center, Sorbonne University INSERM UMR 938; Assistance Publique - Hôpitaux de Paris, Clinical Metabolomics department, Hôpital Saint Antoine, Paris, 75571, France.
Geneviève PilonQuebec Heart and Lung Institute Research Centre, Laval University, Quebec, QC G1V 4G5, Canada.
Josée GauthierDepartment of Medicine, Department of Infectious Diseases and Immunology, and Department of Anatomy and Cell Physiology, University of Florida, Gainesville FL, 32608, USA.
Carole GarofaloDepartment of Nutrition, University of Montreal, Montreal QC H3T 1A8, Canada and Research Centre, Sainte-Justine Hospital, Montreal, QC H3T 1C5, Canada.
Jing X KangLaboratory for Lipid Medicine and Technology, Department of Medicine, Massachusetts General Hospital and Harvard Medical School, Charlestown MA 02129, USA.
Jocelyn TrottierLaboratory of Molecular Pharmacology, CHU-Quebec Research Centre, and Faculty of Pharmacy, Laval University, Quebec, QC G1V 0A6, Canada.
Olivier BarbierLaboratory of Molecular Pharmacology, CHU-Quebec Research Centre, and Faculty of Pharmacy, Laval University, Quebec, QC G1V 0A6, Canada.
Denis RoyFaculty of Agricultural and Food Sciences, School of Nutrition, Laval University, Quebec, QC G1V 0A6, Canada.
Benoit ChassaingINSERM U1016, Mucosal Microbiota in Chronic Inflammatory Diseases' Team, CNRS UMR 8104, University of Paris, Paris, 75014, France.
Emile LevyDepartment of Nutrition, University of Montreal, Montreal QC H3T 1A8, Canada and Research Centre, Sainte-Justine Hospital, Montreal, QC H3T 1C5, Canada.
Frédéric RaymondInstitute of Nutrition and Functional Foods (INAF), Centre NUTRISS, Quebec, QC G1V 0A6, Canada.
Antonin LamaziereSaint Antoine Research Center, Sorbonne University INSERM UMR 938; Assistance Publique - Hôpitaux de Paris, Clinical Metabolomics department, Hôpital Saint Antoine, Paris, 75571, France.ORCID 0000-0003-0813-7370
Nicolas FlamandQuebec Heart and Lung Institute Research Centre, Laval University, Quebec, QC G1V 4G5, Canada.
Cristoforo SilvestriQuebec Heart and Lung Institute Research Centre, Laval University, Quebec, QC G1V 4G5, Canada.
Christian JobinDepartment of Medicine, Department of Infectious Diseases and Immunology, and Department of Anatomy and Cell Physiology, University of Florida, Gainesville FL, 32608, USA.
Vincenzo Di MarzoQuebec Heart and Lung Institute Research Centre, Laval University, Quebec, QC G1V 4G5, Canada.
André MaretteQuebec Heart and Lung Institute Research Centre, Laval University, Quebec, QC G1V 4G5, Canada.ORCID 0000-0003-3950-5973
Université Laval · CACentre Hospitalier Universitaire Sainte-Justine · CAInserm · FRUniversity of Florida · USCentre National de la Recherche Scientifique · FRHarvard University · US

Funding

CIHR FDN-746 143247
6 · The paper itself

Abstract

We compared endogenous ω-3 PUFA production to supplementation for improving obesity-related metabolic dysfunction. Fat-1 transgenic mice, who endogenously convert exogenous ω-6 to ω-3 PUFA, and wild-type littermates were fed a high-fat diet and a daily dose of either ω-3 or ω-6 PUFA-rich oil for 12 wk. The endogenous ω-3 PUFA production improved glucose intolerance and insulin resistance but not hepatic steatosis. Conversely, ω-3 PUFA supplementation fully prevented hepatic steatosis but failed to improve insulin resistance. Both models increased hepatic levels of ω-3 PUFA-containing 2-monoacylglycerol and N-acylethanolamine congeners, and reduced levels of ω-6 PUFA-derived endocannabinoids with ω-3 PUFA supplementation being more efficacious. Reduced hepatic lipid accumulation associated with the endocannabinoidome metabolites EPEA and DHEA, which was causally demonstrated by lower lipid accumulation in oleic acid-treated hepatic cells treated with these metabolites. While both models induced a significant fecal enrichment of the beneficial

Indexed as

Fatty Acids, Omega-3Fatty LiverInsulin ResistanceAnimalsDietary SupplementsMiceMice, TransgenicFatty Acids, Omega-3Allobaculumendocannabinoidsfat-1 genegut-liver axisnonalcoholic fatty liver diseaseω-3 PUFA

Identifiers

PMID36778746
PMCPMC9909367
OpenAlexW4313332679

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.