Evidence map›Paper›PMID 33968013›Full record

ArticleFrontiers in immunology2021

Fish Oil Improves Pathway-Oriented Profiling of Lipid Mediators for Maintaining Metabolic Homeostasis in Adipose Tissue of Prediabetic Rats.

Gabriel Dasilva, Salomé Lois, Lucía Méndez, Bernat Miralles-Pérez, Marta Romeu, Sara Ramos-Romero, Josep L Torres, Isabel Medina

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.5field-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, 16 citations in OpenAlex.

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  11. Dietary Fish Oil Increases the Number of CD11bJournal of inflammation research · 2022
    Article
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.

Gabriel DasilvaFood Science Department, Instituto de Investigaciones Marinas (IIM-CSIC), Vigo, Spain.
Salomé LoisFood Science Department, Instituto de Investigaciones Marinas (IIM-CSIC), Vigo, Spain.
Lucía MéndezFood Science Department, Instituto de Investigaciones Marinas (IIM-CSIC), Vigo, Spain.
Bernat Miralles-PérezUnitat de Farmacologia, Facultat de Medicina i Ciències de la Salut, Universitat Rovira i Virgili, Reus, Spain.
Marta RomeuUnitat de Farmacologia, Facultat de Medicina i Ciències de la Salut, Universitat Rovira i Virgili, Reus, Spain.
Sara Ramos-RomeroBiological Chemistry Department, Instituto de Química Avanzada de Catalunya (IQAC-CSIC), Barcelona, Spain.
Josep L TorresBiological Chemistry Department, Instituto de Química Avanzada de Catalunya (IQAC-CSIC), Barcelona, Spain.
Isabel MedinaFood Science Department, Instituto de Investigaciones Marinas (IIM-CSIC), Vigo, Spain.
Instituto de Investigacións Mariñas · ESInstituto de Química Orgánica General · ESUniversidad Rovira i Virgili · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Adipose tissue is now recognized as an active organ with an important homeostatic function in glucose and lipid metabolism and the development of insulin resistance. The present research investigates the role of lipid mediators and lipid profiling for controlling inflammation and the metabolic normal function of white adipose tissue from rats suffering from diet-induced prediabetes. Additionally, the contribution to the adipose lipidome induced by the consumption of marine ω-3 PUFAs as potential regulators of inflammation is addressed. For that, the effects on the inflammatory response triggered by high-fat high-sucrose (HFHS) diets were studied in male Sprague-Dawley rats. Using SPE-LC-MS/MS-based metabolo-lipidomics, a range of eicosanoids, docosanoids and specialized pro-resolving mediators (SPMs) were measured in white adipose tissue. The inflammatory response occurring in prediabetic adipose tissue was associated with the decomposition of ARA epoxides to ARA-dihydroxides, the reduction of oxo-derivatives and the formation of prostaglandins (PGs). In an attempt to control the inflammatory response initiated, LOX and non-enzymatic oxidation shifted toward the production of the less pro-inflammatory EPA and DHA metabolites rather than the high pro-inflammatory ARA hydroxides. Additionally, the change in LOX activity induced the production of intermediate hydroxides precursors of SPMs as protectins (PDs), resolvins (Rvs) and maresins (MaRs). This compensatory mechanism to achieve the restoration of tissue homeostasis was significantly strengthened through supplementation with fish oils. Increasing proportions of ω-3 PUFAs in adipose tissue significantly stimulated the formation of DHA-epoxides by cytochrome P450, the production of non-enzymatic EPA-metabolites and prompted the activity of 12LOX. Finally, protectin PDX was significantly reduced in the adipose tissue of prediabetic rats and highly enhanced through ω-3 PUFAs supplementation. Taken together, these actively coordinated modifications constitute key mechanisms to restore adipose tissue homeostasis with an important role of lipid mediators. This compensatory mechanism is reinforced through the supplementation of the diet with fish oils with high and balanced contents of EPA and DHA. The study highlights new insides on the targets for effective treatment of incipient diet-induced diabetes and the mechanism underlying the potential anti-inflammatory action of marine lipids.

Indexed as

LipidomicsAdipose TissueAnimalsBiomarkersChromatography, LiquidDietFish OilsHomeostasisInflammation MediatorsLipid MetabolismMaleMetabolic Networks and PathwaysRatsTandem Mass SpectrometryBiomarkersFish OilsInflammation Mediatorsadipose tissueinflammationprediabetesspecialized resolversω3 lipid mediators

Identifiers

PMID33968013
PMCPMC8097180
OpenAlexW3153338418

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.