Evidence map›Paper›PMID 22405074›Full record

ArticleCell metabolism2012

PPARγ agonists induce a white-to-brown fat conversion through stabilization of PRDM16 protein.

Haruya Ohno, Kosaku Shinoda, Bruce M Spiegelman, Shingo Kajimura

Open access · bronzeAbstract read
In one paragraph

Article in Cell metabolism, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 455 papers.

0numbers the graph read from it
0cells of the map it votes in
455citing papers in PubMed
22.6field-weighted citation impact, top 1% 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

455 citing papers in PubMed, 729 citations in OpenAlex.

  1. Article
  2. Review
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  4. Article
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  6. Article
  7. Parathyroid hormone enhances appetite and fails to reduce adiposity in ob/ob mice.Pflugers Archiv : European journal of physiology · 2026
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  8. Caspase-6 Controls Lipid and Energy Metabolism in Diet-Induced Obesity.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
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  9. Article
  10. Mitochondrial control of glycerolipid synthesis by a PEP shuttle.bioRxiv : the preprint server for biology · 2026
    Article
  11. Review
  12. Article
  13. Article
  14. Adipocyte Browning: A Promising Avenue in Anti-Obesity Therapy.International journal of molecular sciences · 2026
    Review
  15. Article
  16. Review
  17. Review
  18. Review
  19. Review
  20. Mitochondrial control of fuel switching via carnitine biosynthesis.bioRxiv : the preprint server for biology · 2025
    Article

395 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

4 authors at 2 institutions in 1 country.

Haruya OhnoUCSF Diabetes Center and Department of Cell and Tissue Biology, University of California, San Francisco, 35 Medical Center Way, San Francisco, CA 94143-0669, USA.
Kosaku Shinoda
Bruce M Spiegelman
Shingo Kajimura
University of California, San Francisco · USHarvard University · US

Funding

Research BaseP30DK063720 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI VAISSE, CHRISTIAN · 2003 to 2019
$21.8M
CONTROL OF ADIPOCYTE GENE EXPRESSION AND PHYSIOLOGYR37DK031405 · NIDDK · DANA-FARBER CANCER INSTITUTE · PI SPIEGELMAN, BRUCE M. · 1996 to 2013
$8.2M
Molecular mechanisms of UCP1-independent pathways in metabolic healthR01DK097441 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI Shingo Kajimura · 2012 to 2026
$5.9M
Regulation of Brown Fat: Toward New Therapy for Human ObesityRC4DK090861 · NIDDK · DANA-FARBER CANCER INST · PI SPIEGELMAN, BRUCE M. · 2010 to 2010
$4.2M
CONTROL OF LIPOGENIC ENZYME SYNTHESIS IN ADIPOCYTESR01DK031405 · NIDDK · DANA-FARBER CANCER INSTITUTE · PI SPIEGELMAN, BRUCE M. · 1986 to 2018
$2.9M
Engineering Functional Brown Fat with Anti-Obesity PotentialR00DK087853 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI KAJIMURA, SHINGO · 2011 to 2013
$634k
Engineering Functional Brown Fat with Anti-Obesity PotentialK99DK087853 · NIDDK · DANA-FARBER CANCER INST · PI KAJIMURA, SHINGO · 2010 to 2011
$135k
NIDDK NIH HHS DK087853NIDDK NIH HHS DK090861NIDDK NIH HHS DK31405NIDDK NIH HHS K99 DK087853NIDDK NIH HHS P30 DK063720NIDDK NIH HHS R00 DK087853NIDDK NIH HHS R01 DK031405NIDDK NIH HHS R01 DK097441NIDDK NIH HHS R37 DK031405NIDDK NIH HHS RC4 DK090861
6 · The paper itself

Abstract

Brown adipose tissue dissipates energy through heat and functions as a defense against cold and obesity. PPARγ ligands have been shown to induce the browning of white adipocytes; however, the underlying mechanisms remain unclear. Here, we show that PPARγ ligands require full agonism to induce a brown fat gene program preferentially in subcutaneous white adipose. These effects require expression of PRDM16, a factor that controls the development of classical brown fat. Depletion of PRDM16 blunts the effects of the PPARγ agonist rosiglitazone on the induced brown fat gene program. Conversely, PRDM16 and rosiglitazone synergistically activate the brown fat gene program in vivo. This synergy is tightly associated with an increased accumulation of PRDM16 protein, due in large measure to an increase in the half-life of the protein in agonist treated cells. Identifying compounds that stabilize PRDM16 protein may represent a plausible therapeutic pathway for the treatment of obesity and diabetes.

Indexed as

Adipose Tissue, BrownAdipose Tissue, WhiteAnimalsBlotting, WesternDNA-Binding ProteinsIndolesMaleMiceMice, Inbred C57BLOxygen ConsumptionPPAR gammaProtein StabilityRosiglitazoneSulfidesThiazolidinedionesTranscription Factors5-chloro-1-(4-chlorobenzyl)-3-(phenylthio)indole-2-carboxylic acidDNA-Binding ProteinsIndolesPPAR gammaPrdm16 protein, mouseRosiglitazoneSulfidesThiazolidinedionesTranscription Factors

Identifiers

PMID22405074
PMCPMC3410936
OpenAlexW2118055379

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.