Evidence map›Paper›PMID 23652116›Full record

ReviewNature medicine2013

PPARγ signaling and metabolism: the good, the bad and the future.

Maryam Ahmadian, Jae Myoung Suh, Nasun Hah, Christopher Liddle, Annette R Atkins, Michael Downes, Ronald M Evans

Abstract readReview
In one paragraph

Review in Nature medicine, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1,087 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
1,087citing papers in PubMed, 3 pooled it
–field-weighted citation impact
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

1,087 citing papers in PubMed, 3 syntheses or guidelines pooled it.

  1. Pooled it
  2. Pooled it
  3. Pollution, stress response, and obesity: A systematic review.Obesity reviews : an official journal of the International Association for the Study of Obesity · 2025
    Pooled it
  4. Trial
  5. Trial
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Review
  12. Dosing PPARγ Activation With Light Using Fast Relaxing Photoswitches.Angewandte Chemie (International ed. in English) · 2026
    Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article

1,027 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

7 authors.

Maryam AhmadianGene Expression Laboratory, Salk Institute for Biological Studies, La Jolla, California, USA.
Jae Myoung Suh
Nasun Hah
Christopher Liddle
Annette R Atkins
Michael Downes
Ronald M Evans

Funding

Yeast Genetics and Stress Response Genes-BiomedicalP42ES010337 · NIEHS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI TUKEY, ROBERT H · 2000 to 2022
$69.8M
Transgenic & Knock-out MouseP30DK063491 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI PETER J TONTONOZ · 2003 to 2026
$40.4M
Transcriptional GenomicsP01HL088093 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI WITZTUM, JOSEPH L. · 2008 to 2018
$26.4M
HORMONAL REGULATION OF MAMMALIAN GENE EXPRESSIONR37DK057978 · NIDDK · SALK INSTITUTE FOR BIOLOGICAL STUDIES · PI EVANS, RONALD M · 2000 to 2019
$16.0M
Spatial Regulation of Developmental Gene ExpressionR01HL105278 · NHLBI · SALK INSTITUTE FOR BIOLOGICAL STUDIES · PI EVANS, RONALD M · 2011 to 2019
$4.0M
Hormonal Regulation of Mammalian Gene ExpressionR01DK057978 · NIDDK · SALK INSTITUTE FOR BIOLOGICAL STUDIES · PI EVANS, RONALD M · 2021 to 2024
$2.6M
Molecular Mechanisms of Inflammation, Steatosis and Hepatic Insulin ResistanceR24DK090962 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI OLEFSKY, JERROLD MICHAEL · 2010 to 2011
$1.5M
Howard Hughes Medical InstituteNHLBI NIH HHS HL088093NHLBI NIH HHS HL105278NHLBI NIH HHS P01 HL088093NHLBI NIH HHS R01 HL105278NIDDK NIH HHS DK057978NIDDK NIH HHS DK090962NIDDK NIH HHS P30 DK063491NIDDK NIH HHS R01 DK057978NIDDK NIH HHS R24 DK090962NIDDK NIH HHS R37 DK057978NIEHS NIH HHS ES010337NIEHS NIH HHS P42 ES010337
6 · The paper itself

Abstract

Thiazolidinediones (TZDs) are potent insulin sensitizers that act through the nuclear receptor peroxisome proliferator-activated receptor-γ (PPARγ) and are highly effective oral medications for type 2 diabetes. However, their unique benefits are shadowed by the risk for fluid retention, weight gain, bone loss and congestive heart failure. This raises the question as to whether it is possible to build a safer generation of PPARγ-specific drugs that evoke fewer side effects while preserving insulin-sensitizing potential. Recent studies that have supported the continuing physiologic and therapeutic relevance of the PPARγ pathway also provide opportunities to develop newer classes of molecules that reduce or eliminate adverse effects. This review highlights key advances in understanding PPARγ signaling in energy homeostasis and metabolic disease and also provides new explanations for adverse events linked to TZD-based therapy.

Indexed as

Adipose TissueAnimalsFatty AcidsFibroblast Growth FactorsHomeostasisHumansHypoglycemic AgentsInsulinMiceMolecular Targeted TherapyPPAR gammaProtein Processing, Post-TranslationalSignal TransductionThiazolidinedionesFatty AcidsFibroblast Growth FactorsHypoglycemic AgentsInsulinPPAR gammaThiazolidinediones

Identifiers

PMID23652116
PMCPMC3870016

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.