Evidence map›Paper›PMID 33397965›Full record

ArticleNature communications2021

Deletion of Trim28 in committed adipocytes promotes obesity but preserves glucose tolerance.

Simon T Bond, Emily J King, Darren C Henstridge, Adrian Tran, Sarah C Moody, Christine Yang, Yingying Liu, Natalie A Mellett, Artika P Nath, Michael Inouye and 5 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
2.8field-weighted citation impact, top 9% 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

18 citing papers in PubMed, 31 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

15 authors at 3 institutions in 3 countries.

Simon T BondBaker Heart & Diabetes Institute, Melbourne, VIC, Australia, 3004.ORCID 0000-0003-1551-8614
Emily J KingBaker Heart & Diabetes Institute, Melbourne, VIC, Australia, 3004.ORCID 0000-0002-4950-5662
Darren C HenstridgeBaker Heart & Diabetes Institute, Melbourne, VIC, Australia, 3004.ORCID 0000-0003-4988-767X
Adrian TranBaker Heart & Diabetes Institute, Melbourne, VIC, Australia, 3004.ORCID 0000-0002-9622-1486
Sarah C MoodyBaker Heart & Diabetes Institute, Melbourne, VIC, Australia, 3004.ORCID 0000-0003-4478-142X
Christine YangBaker Heart & Diabetes Institute, Melbourne, VIC, Australia, 3004.
Yingying LiuBaker Heart & Diabetes Institute, Melbourne, VIC, Australia, 3004.
Natalie A MellettBaker Heart & Diabetes Institute, Melbourne, VIC, Australia, 3004.
Artika P NathBaker Heart & Diabetes Institute, Melbourne, VIC, Australia, 3004.
Michael InouyeBaker Heart & Diabetes Institute, Melbourne, VIC, Australia, 3004.
Elizabeth J TarlingDepartment of Medicine, University of California Los Angeles, Los Angeles, CA, USA.ORCID 0000-0002-0599-0432
Thomas Q de Aguiar VallimDepartment of Medicine, University of California Los Angeles, Los Angeles, CA, USA.
Peter J MeikleBaker Heart & Diabetes Institute, Melbourne, VIC, Australia, 3004.ORCID 0000-0002-2593-4665
Anna C CalkinBaker Heart & Diabetes Institute, Melbourne, VIC, Australia, 3004.
Brian G DrewBaker Heart & Diabetes Institute, Melbourne, VIC, Australia, 3004. brian.drew@baker.edu.au.ORCID 0000-0002-7839-9467
Baker Heart and Diabetes Institute · AUUniversity of California, Los Angeles · USUniversity of Tasmania · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The effective storage of lipids in white adipose tissue (WAT) critically impacts whole body energy homeostasis. Many genes have been implicated in WAT lipid metabolism, including tripartite motif containing 28 (Trim28), a gene proposed to primarily influence adiposity via epigenetic mechanisms in embryonic development. However, in the current study we demonstrate that mice with deletion of Trim28 specifically in committed adipocytes, also develop obesity similar to global Trim28 deletion models, highlighting a post-developmental role for Trim28. These effects were exacerbated in female mice, contributing to the growing notion that Trim28 is a sex-specific regulator of obesity. Mechanistically, this phenotype involves alterations in lipolysis and triglyceride metabolism, explained in part by loss of Klf14 expression, a gene previously demonstrated to modulate adipocyte size and body composition in a sex-specific manner. Thus, these findings provide evidence that Trim28 is a bona fide, sex specific regulator of post-developmental adiposity and WAT function.

Indexed as

Gene Deletion3T3-L1 CellsAdipocytesAdipose Tissue, WhiteAdiposityAnimalsBody WeightDietDiet, High-FatEnergy MetabolismFemaleGene Regulatory NetworksGlucoseLipid MetabolismMaleMiceGlucoseTriglyceridesTrim28 protein, mouseTripartite Motif-Containing Protein 28

Identifiers

PMID33397965
PMCPMC7782476
OpenAlexW3118365598

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.