Evidence map›Paper›PMID 26118629›Full record

ArticleNature communications2015

Cidea improves the metabolic profile through expansion of adipose tissue.

Gustavo Abreu-Vieira, Alexander W Fischer, Charlotte Mattsson, Jasper M A de Jong, Irina G Shabalina, Mikael Rydén, Jurga Laurencikiene, Peter Arner, Barbara Cannon, Jan Nedergaard and 1 more

Erratum issuedOpen access · goldAbstract read
PubMed Publisher
In one paragraph

Article in Nature communications, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 67 papers.

0numbers the graph read from it
0cells of the map it votes in
67citing papers in PubMed
5.3field-weighted citation impact, top 4% 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

67 citing papers in PubMed, 102 citations in OpenAlex.

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7 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

11 authors at 2 institutions in 1 country.

Gustavo Abreu-VieiraDepartment of Molecular Biosciences, Wenner-Gren Institute, Arrhenius Laboratories F3, Stockholm University, 106 91 Stockholm, Sweden.
Alexander W Fischer1] Department of Molecular Biosciences, Wenner-Gren Institute, Arrhenius Laboratories F3, Stockholm University, 106 91 Stockholm, Sweden [2] Department of Biochemistry and Molecular Cell Biology, University Medical Center Hamburg-Eppendorf, 20246 Hamburg, Germany.
Charlotte MattssonDepartment of Cell and Molecular Biology, Karolinska Institutet, 171 77 Stockholm, Sweden.
Jasper M A de JongDepartment of Molecular Biosciences, Wenner-Gren Institute, Arrhenius Laboratories F3, Stockholm University, 106 91 Stockholm, Sweden.
Irina G ShabalinaDepartment of Molecular Biosciences, Wenner-Gren Institute, Arrhenius Laboratories F3, Stockholm University, 106 91 Stockholm, Sweden.
Mikael RydénDepartment of Medicine, Huddinge, Lipid Laboratory, Karolinska Institutet, 141 86 Stockholm, Sweden.
Jurga LaurencikieneDepartment of Medicine, Huddinge, Lipid Laboratory, Karolinska Institutet, 141 86 Stockholm, Sweden.
Peter ArnerDepartment of Medicine, Huddinge, Lipid Laboratory, Karolinska Institutet, 141 86 Stockholm, Sweden.
Barbara CannonDepartment of Molecular Biosciences, Wenner-Gren Institute, Arrhenius Laboratories F3, Stockholm University, 106 91 Stockholm, Sweden.
Jan NedergaardDepartment of Molecular Biosciences, Wenner-Gren Institute, Arrhenius Laboratories F3, Stockholm University, 106 91 Stockholm, Sweden.
Natasa PetrovicDepartment of Molecular Biosciences, Wenner-Gren Institute, Arrhenius Laboratories F3, Stockholm University, 106 91 Stockholm, Sweden.
Stockholm University · SEKarolinska Institutet · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In humans, Cidea (cell death-inducing DNA fragmentation factor alpha-like effector A) is highly but variably expressed in white fat, and expression correlates with metabolic health. Here we generate transgenic mice expressing human Cidea in adipose tissues (aP2-hCidea mice) and show that Cidea is mechanistically associated with a robust increase in adipose tissue expandability. Under humanized conditions (thermoneutrality, mature age and prolonged exposure to high-fat diet), aP2-hCidea mice develop a much more pronounced obesity than their wild-type littermates. Remarkably, the malfunctioning of visceral fat normally caused by massive obesity is fully overcome-perilipin 1 and Akt expression are preserved, tissue degradation is prevented, macrophage accumulation is decreased and adiponectin expression remains high. Importantly, the aP2-hCidea mice display enhanced insulin sensitivity. Our data establish a functional role for Cidea and suggest that, in humans, the association between Cidea levels in white fat and metabolic health is not only correlative but also causative.

Indexed as

Adipose TissueAnimalsApoptosis Regulatory ProteinsDietary FatsEnergy MetabolismGene Expression RegulationGenotypeInsulin ResistanceMacrophagesMiceMice, TransgenicApoptosis Regulatory ProteinsCIDEA protein, humanDietary Fats

Identifiers

PMID26118629
OpenAlexW1635675251

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.