Evidence map›Paper›PMID 29320702›Full record

ArticleCell metabolism2018

Repression of Adipose Tissue Fibrosis through a PRDM16-GTF2IRD1 Complex Improves Systemic Glucose Homeostasis.

Yutaka Hasegawa, Kenji Ikeda, Yong Chen, Diana L Alba, Daniel Stifler, Kosaku Shinoda, Takashi Hosono, Pema Maretich, Yangyu Yang, Yasushi Ishigaki and 4 more

Open access · bronzeAbstract read
In one paragraph

Article in Cell metabolism, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 110 papers.

0numbers the graph read from it
0cells of the map it votes in
110citing papers in PubMed
6.2field-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

110 citing papers in PubMed, 184 citations in OpenAlex.

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  11. Ablation ofScience (New York, N.Y.) · 2026
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50 more citing papers are in PubMed but not listed here.

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 4 institutions in 2 countries.

Yutaka HasegawaUCSF Diabetes Center, San Francisco, CA, USA; Eli and Edythe Broad Center of Regeneration Medicine and Stem Cell Research, San Francisco, CA, USA; Department of Cell and Tissue Biology, University of California, San Francisco, San Francisco, CA, USA; Division of Diabetes and Metabolism, Department of Internal Medicine, Iwate Medical University, Morioka, Uchimaru, Japan.
Kenji IkedaUCSF Diabetes Center, San Francisco, CA, USA; Eli and Edythe Broad Center of Regeneration Medicine and Stem Cell Research, San Francisco, CA, USA; Department of Cell and Tissue Biology, University of California, San Francisco, San Francisco, CA, USA.
Yong ChenUCSF Diabetes Center, San Francisco, CA, USA; Eli and Edythe Broad Center of Regeneration Medicine and Stem Cell Research, San Francisco, CA, USA; Department of Cell and Tissue Biology, University of California, San Francisco, San Francisco, CA, USA.
Diana L AlbaUCSF Diabetes Center, San Francisco, CA, USA; Department of Medicine, University of California, San Francisco, San Francisco, CA, USA.
Daniel StiflerUCSF Diabetes Center, San Francisco, CA, USA; Department of Medicine, University of California, San Francisco, San Francisco, CA, USA.
Kosaku ShinodaUCSF Diabetes Center, San Francisco, CA, USA; Eli and Edythe Broad Center of Regeneration Medicine and Stem Cell Research, San Francisco, CA, USA; Department of Cell and Tissue Biology, University of California, San Francisco, San Francisco, CA, USA.
Takashi HosonoUCSF Diabetes Center, San Francisco, CA, USA; Eli and Edythe Broad Center of Regeneration Medicine and Stem Cell Research, San Francisco, CA, USA; Department of Cell and Tissue Biology, University of California, San Francisco, San Francisco, CA, USA; Department of Chemistry and Life Science, College of Bioresource Sciences, Nihon University, Tokyo, Japan.
Pema MaretichUCSF Diabetes Center, San Francisco, CA, USA; Eli and Edythe Broad Center of Regeneration Medicine and Stem Cell Research, San Francisco, CA, USA; Department of Cell and Tissue Biology, University of California, San Francisco, San Francisco, CA, USA.
Yangyu YangUCSF Diabetes Center, San Francisco, CA, USA; Eli and Edythe Broad Center of Regeneration Medicine and Stem Cell Research, San Francisco, CA, USA; Department of Cell and Tissue Biology, University of California, San Francisco, San Francisco, CA, USA.
Yasushi IshigakiDivision of Diabetes and Metabolism, Department of Internal Medicine, Iwate Medical University, Morioka, Uchimaru, Japan.
Jingyi ChiThe Rockefeller University, Laboratory of Molecular Metabolism, New York, NY, USA.
Paul CohenThe Rockefeller University, Laboratory of Molecular Metabolism, New York, NY, USA.
Suneil K KoliwadUCSF Diabetes Center, San Francisco, CA, USA; Department of Medicine, University of California, San Francisco, San Francisco, CA, USA. Electronic address: suneil.koliwad2@ucsf.edu.
Shingo KajimuraUCSF Diabetes Center, San Francisco, CA, USA; Eli and Edythe Broad Center of Regeneration Medicine and Stem Cell Research, San Francisco, CA, USA; Department of Cell and Tissue Biology, University of California, San Francisco, San Francisco, CA, USA. Electronic address: shingo.kajimura@ucsf.edu.
Broad Center · USUniversity of California, San Francisco · USRockefeller University · USIwate Medical University · JP

Funding

Virology CoreP30AI027763 · NIAID · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI STEVEN Grant DEEKS · 1988 to 2026
$93.6M
RESEARCH TRAININGP30DK026687 · NIDDK · ST. LUKE'S-ROOSEVELT INST FOR HLTH SCIS · PI Anthony W Ferrante, DYMPNA GALLAGHER · 1986 to 2026
$33.0M
Translational Research CoreP30DK020541 · NIDDK · ALBERT EINSTEIN COLLEGE OF MEDICINE, INC · PI STREAMSON C CHUA · 2015 to 2026
$27.7M
Research BaseP30DK063720 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI KRUMMEL, MATTHEW F · 2003 to 2019
$21.8M
UCSF Nutrition Obesity Research CenterP30DK098722 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI CHRISTIAN VAISSE · 2015 to 2026
$14.6M
DIABETES, ENDOCRINOLOGY &METABOLISM TRAINING PROGRAMT32DK007418 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI EDWARD C HSIAO · 1986 to 2026
$14.3M
Molecular mechanisms of UCP1-independent pathways in metabolic healthR01DK097441 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI Shingo Kajimura · 2012 to 2026
$5.9M
Immunologic and Fat-Associated Predictors of Insulin Resistance in Treated HIVR01DK112304 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI HUNT, PETER W, KOLIWAD, SUNEIL KRISHNA · 2017 to 2021
$4.1M
Microglia: dietary fat-sensitive mediators of inflammation and metabolic diseaseR01DK103175 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI KOLIWAD, SUNEIL KRISHNA · 2015 to 2019
$1.8M
BAT-mediated inter-organ communication in energy homeostasisR01DK108822 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI KAJIMURA, SHINGO · 2016 to 2019
$1.4M
NIAID NIH HHS P30 AI027763NIDDK NIH HHS P30 DK020541NIDDK NIH HHS P30 DK026687NIDDK NIH HHS P30 DK063720NIDDK NIH HHS P30 DK098722NIDDK NIH HHS R01 DK097441NIDDK NIH HHS R01 DK103175NIDDK NIH HHS R01 DK108822NIDDK NIH HHS R01 DK112304NIDDK NIH HHS T32 DK007418
6 · The paper itself

Abstract

Adipose tissue fibrosis is a hallmark of malfunction that is linked to insulin resistance and type 2 diabetes; however, what regulates this process remains unclear. Here we show that the PRDM16 transcriptional complex, a dominant activator of brown/beige adipocyte development, potently represses adipose tissue fibrosis in an uncoupling protein 1 (UCP1)-independent manner. By purifying the PRDM16 complex, we identified GTF2IRD1, a member of the TFII-I family of DNA-binding proteins, as a cold-inducible transcription factor that mediates the repressive action of the PRDM16 complex on fibrosis. Adipocyte-selective expression of GTF2IRD1 represses adipose tissue fibrosis and improves systemic glucose homeostasis independent of body-weight loss, while deleting GTF2IRD1 promotes fibrosis in a cell-autonomous manner. GTF2IRD1 represses the transcription of transforming growth factor β-dependent pro-fibrosis genes by recruiting PRDM16 and EHMT1 onto their promoter/enhancer regions. These results suggest a mechanism by which repression of obesity-associated adipose tissue fibrosis through the PRDM16 complex leads to an improvement in systemic glucose homeostasis.

Indexed as

HomeostasisAdipocytesAdipose TissueAdipose Tissue, BrownAnimalsBody WeightDietDNA-Binding ProteinsFibrosisGene Expression RegulationGlucoseHistone-Lysine N-MethyltransferaseInsulin ResistanceMice, TransgenicMuscle ProteinsNuclear ProteinsDNA-Binding ProteinsGLP protein, mouseGlucoseGtf2ird1 protein, mouseHistone-Lysine N-MethyltransferaseMuscle ProteinsNuclear ProteinsPrdm16 protein, mouseTrans-ActivatorsTranscription FactorsUncoupling Protein 1adipose tissue fibrosisbeige adipocytebrown adipose tissuediabetesEHMT1GTF2IRD1insulin resistanceobesityPRDM16UCP1-independent

Identifiers

PMID29320702
PMCPMC5765755
OpenAlexW2783764158

What OpenQuestion holds

Textmetadata
LicenceTDM
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.