Evidence map›Paper›PMID 22843443›Full record

ArticleEuropean heart journal2013

Activation of intestinal peroxisome proliferator-activated receptor-α increases high-density lipoprotein production.

Sophie Colin, Olivier Briand, Véronique Touche, Kristiaan Wouters, Morgane Baron, François Pattou, Rémy Hanf, Anne Tailleux, Giulia Chinetti, Bart Staels and 1 more

Open access · greenAbstract read
In one paragraph

Article in European heart journal, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed, 1 pooled it
1.5field-weighted citation impact, top 18% 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

31 citing papers in PubMed, 1 synthesis or guideline pooled it, 63 citations in OpenAlex.

  1. Pooled it
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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

11 authors at 5 institutions in 1 country.

Sophie ColinUniversité Lille Nord de France, Lille F-59000, France.
Olivier Briand
Véronique Touche
Kristiaan Wouters
Morgane Baron
François Pattou
Rémy Hanf
Anne Tailleux
Giulia Chinetti
Bart Staels
Sophie Lestavel
Université de Lille · FRUniversité Lille Nord de France · FRInserm · FRInstitut Pasteur de Lille · FRGenfit (France) · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aimsPeroxisome proliferator-activated receptor (PPAR)-α is a transcription factor controlling lipid metabolism in liver, heart, muscle, and macrophages. Peroxisome proliferator-activated receptor-α activation increases plasma HDL cholesterol and exerts hypotriglyceridaemic actions via the liver. However, the intestine expresses PPAR-α, produces HDL and chylomicrons, and is exposed to diet-derived PPAR-α ligands. Therefore, we examined the effects of PPAR-α activation on intestinal lipid and lipoprotein metabolism. METHODS AND

resultsThe impact of PPAR-α activation was evaluated in term of HDL-related gene expression in mice, ex vivo in human jejunal biopsies and in Caco-2/TC7 cells. Apolipoprotein-AI/HDL secretion, cholesterol esterification, and trafficking were also studied in vitro. In parallel to improving plasma lipid profiles and increasing liver and intestinal expression of fatty acid oxidation genes, treatment with the dual PPAR-α/δ ligand GFT505 resulted in a more pronounced increase in plasma HDL compared with fenofibrate in mice. GFT505, but not fenofibrate, increased the expression of HDL production genes such as apolipoprotein-AI and ATP-binding cassette A1 transporter in murine intestines. A similar increase was observed upon PPAR-α activation of human biopsies and Caco-2/TC7 cells. Additionally, HDL secretion by Caco-2/TC7 cells increased. Moreover, PPAR-α activation decreased the cholesterol esterification capacity of Caco-2/TC7 cells, modified cholesterol trafficking, and reduced apolipoprotein-B secretion.

conclusionPeroxisome proliferator-activated receptor-α activation reduces cholesterol esterification, suppresses chylomicron, and increases HDL secretion by enterocytes. These results identify the intestine as a target organ of PPAR-α ligands with entero-hepatic tropism to reduce atherogenic dyslipidaemia.

Indexed as

AnimalsApolipoproteins BButyratesCaco-2 CellsCells, CulturedChalconesEnterocytesEsterificationFatty AcidsFemaleHumansJejunumLipoproteins, HDLMiceMice, KnockoutPhenylurea Compounds2-(2,6-dimethyl-4-(3-(4-(methylthio)phenyl)-3-oxo-1-propenyl)phenoxyl)-2-methylpropanoic acidApolipoproteins BButyratesChalconesFatty AcidsGW 7647Lipoproteins, HDLPhenylurea CompoundsPPAR alphaPropionatesDyslipidaemiaHDLIntestinePPAR-α

Identifiers

PMID22843443
PMCPMC3984589
OpenAlexW2168221683

What OpenQuestion holds

Textmetadata
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.