Evidence map›Paper›PMID 32176696›Full record

ArticlePloS one2020

The PPAR pan-agonist tetradecylthioacetic acid promotes redistribution of plasma cholesterol towards large HDL.

Thomas Lundåsen, Matteo Pedrelli, Bodil Bjørndal, Björn Rozell, Raoul V Kuiper, Lena Burri, Chiara Pavanello, Marta Turri, Jon Skorve, Rolf K Berge and 2 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.4field-weighted citation impact, top 41% 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

1 citing paper in PubMed, 6 citations in OpenAlex.

  1. 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

12 authors at 5 institutions in 3 countries.

Thomas LundåsenDepartment of Laboratory Medicine, Karolinska Institutet, Huddinge, Sweden.
Matteo PedrelliDepartment of Laboratory Medicine, Karolinska Institutet, Huddinge, Sweden.
Bodil BjørndalDepartment of Clinical Science, University of Bergen, Bergen, Norway.
Björn RozellDepartment of Laboratory Medicine, Karolinska Institutet, Huddinge, Sweden.
Raoul V KuiperDepartment of Laboratory Medicine, Karolinska Institutet, Huddinge, Sweden.
Lena BurriDepartment of Clinical Science, University of Bergen, Bergen, Norway.
Chiara PavanelloDipartimento di Scienze Farmacologiche e Biomolecolari, Centro Enrica Grossi Paoletti, Università degli Studi di Milano, Milan, Italy.
Marta TurriDipartimento di Scienze Farmacologiche e Biomolecolari, Centro Enrica Grossi Paoletti, Università degli Studi di Milano, Milan, Italy.
Jon SkorveDepartment of Clinical Science, University of Bergen, Bergen, Norway.
Rolf K BergeDepartment of Clinical Science, University of Bergen, Bergen, Norway.
Stefan E H AlexsonDepartment of Laboratory Medicine, Karolinska Institutet, Huddinge, Sweden.
Veronika TillanderDepartment of Laboratory Medicine, Karolinska Institutet, Huddinge, Sweden.ORCID 0000-0002-2134-7164
Karolinska Institutet · SEUniversity of Bergen · NOUniversity of Milan · ITHaukeland University Hospital · NOWestern Norway University of Applied Sciences · NO

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Tetradecylthioacetic acid (TTA) is a synthetic fatty acid with a sulfur substitution in the β-position. This modification renders TTA unable to undergo complete β-oxidation and increases its biological activity, including activation of peroxisome proliferator activated receptors (PPARs) with preference for PPARα. This study investigated the effects of TTA on lipid and lipoprotein metabolism in the intestine and liver of mice fed a high fat diet (HFD). Mice receiving HFD supplemented with 0.75% (w/w) TTA had significantly lower body weights compared to mice fed the diet without TTA. Plasma triacylglycerol (TAG) was reduced 3-fold with TTA treatment, concurrent with increase in liver TAG. Total cholesterol was unchanged in plasma and liver. However, TTA promoted a shift in the plasma lipoprotein fractions with an increase in larger HDL particles. Histological analysis of the small intestine revealed a reduced size of lipid droplets in enterocytes of TTA treated mice, accompanied by increased mRNA expression of fatty acid transporter genes. Expression of the cholesterol efflux pump Abca1 was induced in the small intestine, but not in the liver. Scd1 displayed markedly increased mRNA and protein expression in the intestine of the TTA group. It is concluded that TTA treatment of HFD fed mice leads to increased expression of genes involved in uptake and transport of fatty acids and HDL cholesterol in the small intestine with concomitant changes in the plasma profile of smaller lipoproteins.

Indexed as

AnimalsATP Binding Cassette Transporter 1Body WeightCholesterol, HDLDiet, High-FatIntestinal MucosaLipid MetabolismLipoproteinsLiverMaleMicePPAR alphaStearoyl-CoA DesaturaseSulfidesTriglycerides1-(carboxymethylthio)tetradecaneAbca1 protein, mouseATP Binding Cassette Transporter 1Cholesterol, HDLLipoproteinsPPAR alphaPpara protein, mouseScd1 protein, mouseStearoyl-CoA DesaturaseSulfidesTriglycerides

Identifiers

PMID32176696
PMCPMC7075573
OpenAlexW3012474373

What OpenQuestion holds

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LicenceCC BY
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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.