Evidence map›Paper›PMID 27922115›Full record

ArticleScientific reports2016

Perilipin 5 fine-tunes lipid oxidation to metabolic demand and protects against lipotoxicity in skeletal muscle.

Claire Laurens, Virginie Bourlier, Aline Mairal, Katie Louche, Pierre-Marie Badin, Etienne Mouisel, Alexandra Montagner, André Marette, Angelo Tremblay, John S Weisnagel and 4 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.

0numbers the graph read from it
0cells of the map it votes in
55citing papers in PubMed
7.5field-weighted citation impact, top 3% 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

55 citing papers in PubMed, 92 citations in OpenAlex.

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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

14 authors at 7 institutions in 2 countries.

Claire LaurensINSERM, UMR1048, Institute of Metabolic and Cardiovascular Diseases, Toulouse, France.
Virginie BourlierINSERM, UMR1048, Institute of Metabolic and Cardiovascular Diseases, Toulouse, France.
Aline MairalINSERM, UMR1048, Institute of Metabolic and Cardiovascular Diseases, Toulouse, France.
Katie LoucheINSERM, UMR1048, Institute of Metabolic and Cardiovascular Diseases, Toulouse, France.
Pierre-Marie BadinINSERM, UMR1048, Institute of Metabolic and Cardiovascular Diseases, Toulouse, France.
Etienne MouiselINSERM, UMR1048, Institute of Metabolic and Cardiovascular Diseases, Toulouse, France.
Alexandra MontagnerUniversity of Toulouse, Paul Sabatier University, France.
André MaretteDepartment of Medicine, Laval University, Quebec City, Canada.
Angelo TremblayCentre de Recherche de l'Institut Universitaire de Cardiologie et de Pneumologie de Québec, Laval University, Quebec City, Canada.
John S WeisnagelCHU-CHUQ, Laval University, Quebec City, Canada.
Hervé GuillouUniversity of Toulouse, Paul Sabatier University, France.
Dominique LanginINSERM, UMR1048, Institute of Metabolic and Cardiovascular Diseases, Toulouse, France.
Denis R JoanisseCentre de Recherche de l'Institut Universitaire de Cardiologie et de Pneumologie de Québec, Laval University, Quebec City, Canada.
Cedric MoroINSERM, UMR1048, Institute of Metabolic and Cardiovascular Diseases, Toulouse, France.
Université Toulouse III - Paul Sabatier · FRInstitut des Maladies Métaboliques et Cardiovasculaires · FRInstitut universitaire de cardiologie et de pneumologie de Québec · CAUniversité Laval · CAInserm · FRToxalim Research Centre in Food Toxicology · FRUniversité Fédérale de Toulouse Midi-Pyrénées · FR

Funding

CIHR MOP-68846
6 · The paper itself

Abstract

Lipid droplets (LD) play a central role in lipid homeostasis by controlling transient fatty acid (FA) storage and release from triacylglycerols stores, while preventing high levels of cellular toxic lipids. This crucial function in oxidative tissues is altered in obesity and type 2 diabetes. Perilipin 5 (PLIN5) is a LD protein whose mechanistic and causal link with lipotoxicity and insulin resistance has raised controversies. We investigated here the physiological role of PLIN5 in skeletal muscle upon various metabolic challenges. We show that PLIN5 protein is elevated in endurance-trained (ET) subjects and correlates with muscle oxidative capacity and whole-body insulin sensitivity. When overexpressed in human skeletal muscle cells to recapitulate the ET phenotype, PLIN5 diminishes lipolysis and FA oxidation under basal condition, but paradoxically enhances FA oxidation during forskolin- and contraction- mediated lipolysis. Moreover, PLIN5 partly protects muscle cells against lipid-induced lipotoxicity. In addition, we demonstrate that down-regulation of PLIN5 in skeletal muscle inhibits insulin-mediated glucose uptake under normal chow feeding condition, while paradoxically improving insulin sensitivity upon high-fat feeding. These data highlight a key role of PLIN5 in LD function, first by finely adjusting LD FA supply to mitochondrial oxidation, and second acting as a protective factor against lipotoxicity in skeletal muscle.

Indexed as

AnimalsBody WeightDiglyceridesGene ExpressionHumansInsulin ResistanceLipid DropletsLipolysisMaleMiceMice, Inbred C57BLMitochondriaMuscle, SkeletalOleic AcidOxidation-ReductionPerilipin-5DiglyceridesOleic AcidPerilipin-5PLIN5 protein, humanPlin5 protein, mouseTriglycerides

Identifiers

PMID27922115
PMCPMC5138838
OpenAlexW2560184119

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.