Evidence map›Paper›PMID 24986106›Full record

ArticleScientific reports2014

PPARα-independent actions of omega-3 PUFAs contribute to their beneficial effects on adiposity and glucose homeostasis.

Menghan Liu, Magdalene K Montgomery, Corrine E Fiveash, Brenna Osborne, Gregory J Cooney, Kim Bell-Anderson, Nigel Turner

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed, 1 pooled it
1.9field-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

14 citing papers in PubMed, 1 synthesis or guideline pooled it, 20 citations in OpenAlex.

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  10. Metabolomic Evaluation ofNutrients · 2019
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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

7 authors at 3 institutions in 1 country.

Menghan Liu1] Diabetes & Obesity Research Program, Garvan Institute of Medical Research, Darlinghurst, NSW, Australia [2] Department of Pharmacology, School of Medical Sciences, University of New South Wales, Sydney, NSW, Australia [3] School of Molecular Bioscience, University of Sydney, Sydney, NSW 2006, Australia.
Magdalene K Montgomery1] Diabetes & Obesity Research Program, Garvan Institute of Medical Research, Darlinghurst, NSW, Australia [2] Department of Pharmacology, School of Medical Sciences, University of New South Wales, Sydney, NSW, Australia.
Corrine E FiveashDepartment of Pharmacology, School of Medical Sciences, University of New South Wales, Sydney, NSW, Australia.
Brenna OsborneDiabetes & Obesity Research Program, Garvan Institute of Medical Research, Darlinghurst, NSW, Australia.
Gregory J Cooney1] Diabetes & Obesity Research Program, Garvan Institute of Medical Research, Darlinghurst, NSW, Australia [2] St Vincent's Clinical School, University of New South Wales, Sydney, NSW, Australia.
Kim Bell-AndersonSchool of Molecular Bioscience, University of Sydney, Sydney, NSW 2006, Australia.
Nigel Turner1] Diabetes & Obesity Research Program, Garvan Institute of Medical Research, Darlinghurst, NSW, Australia [2] Department of Pharmacology, School of Medical Sciences, University of New South Wales, Sydney, NSW, Australia.
Garvan Institute of Medical Research · AUUniversity of Sydney · AUUNSW Sydney · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Excess dietary lipid generally leads to fat deposition and impaired glucose homeostasis, but consumption of fish oil (FO) alleviates many of these detrimental effects. The beneficial effects of FO are thought to be mediated largely via activation of the nuclear receptor peroxisomal-proliferator-activated receptor α (PPARα) by omega-3 polyunsaturated fatty acids and the resulting upregulation of lipid catabolism. However, pharmacological and genetic PPARα manipulations have yielded variable results. We have compared the metabolic effects of FO supplementation and the synthetic PPARα agonist Wy-14,643 (WY) in mice fed a lard-based high-fat diet. In contrast to FO, WY treatment resulted in little protection against diet-induced obesity and glucose intolerance, despite upregulating many lipid metabolic pathways. These differences were likely due to differential effects on hepatic lipid synthesis, with FO decreasing and WY amplifying hepatic lipid accumulation. Our results highlight that the beneficial metabolic effects of FO are likely mediated through multiple independent pathways.

Indexed as

Adipose TissueAdiposityAdministration, OralAnimalsDietary SupplementsDose-Response Relationship, DrugFatty Acids, Omega-3Fish OilsGlucose IntoleranceHomeostasisMaleMiceMice, Inbred C57BLObesityPPAR alphaTreatment OutcomeFatty Acids, Omega-3Fish OilsPPAR alpha

Identifiers

PMID24986106
PMCPMC4078310
OpenAlexW2007346833

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.