Evidence map›Paper›PMID 22078880›Full record

ArticleCell2011

Adipocyte NCoR knockout decreases PPARγ phosphorylation and enhances PPARγ activity and insulin sensitivity.

Pingping Li, Wuqiang Fan, Jianfeng Xu, Min Lu, Hiroyasu Yamamoto, Johan Auwerx, Dorothy D Sears, Saswata Talukdar, DaYoung Oh, Ai Chen and 5 more

Open access · bronzeAbstract read
In one paragraph

Article in Cell, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 170 papers.

0numbers the graph read from it
0cells of the map it votes in
170citing papers in PubMed
14.9field-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

170 citing papers in PubMed, 267 citations in OpenAlex.

  1. Trial
  2. Trial
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Review
  19. Review
  20. A structural mechanism of nuclear receptor biased agonism.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article

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

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

15 authors at 2 institutions in 2 countries.

Pingping LiDivision of Endocrinology and Metabolism, Department of Medicine, University of California, San Diego, 9500 Gilman Drive, La Jolla, CA 92093, USA.
Wuqiang Fan
Jianfeng Xu
Min Lu
Hiroyasu Yamamoto
Johan Auwerx
Dorothy D Sears
Saswata Talukdar
DaYoung Oh
Ai Chen
Gautam Bandyopadhyay
Miriam Scadeng
Jachelle M Ofrecio
Sarah Nalbandian
Jerrold M Olefsky
University of California San Diego · USÉcole Polytechnique Fédérale de Lausanne · CH

Funding

Transgenic & Knock-out MouseP30DK063491 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI PETER J TONTONOZ · 2003 to 2026
$40.4M
TISSUE COACTIVATOR AND RECEPTOR EXPRESSION FINGERPRINTSP01DK059820 · NIDDK · INSTITUT DE GENETIQUE ET BIOLOGIE MOLECU · PI O'MALLEY, BERT W · 2001 to 2016
$23.1M
The Interaction of Neuroendocrine Repro. Function and Metabolic SignalingU54HD012303 · NICHD · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI MELLON, PAMELA L · 1999 to 2013
$18.0M
Transcriptional Genomics CoreP01DK074868 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI GLASS, CHRISTOPHER K · 2007 to 2016
$16.6M
The Role of FSH in Female InfertilityP50HD012303 · NICHD · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI MELLON, PAMELA L · 1985 to 2020
$7.5M
INSULIN RECEPTORS AND THE GLUCOSE TRANSPORT SYSTEMR37DK033651 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI OLEFSKY, JERROLD MICHAEL · 2000 to 2010
$6.1M
TRAINING PROGRAM IN DIABETES RESEARCHT32DK007494 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI SALTIEL, ALAN R. · 1986 to 2021
$4.7M
INSULIN RECEPTORS AND THE GLUCOSE TRANSPORT SYSTEMR01DK033651 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI OLEFSKY, JERROLD MICHAEL · 1986 to 2013
$2.2M
European Research Council 231138NICHD NIH HHS P50 HD012303NICHD NIH HHS U54 HD012303NICHD NIH HHS U54 HD 012303-25NIDDK NIH HHS DK033651NIDDK NIH HHS DK059820NIDDK NIH HHS DK063491NIDDK NIH HHS DK 074868NIDDK NIH HHS P01 DK059820NIDDK NIH HHS P01 DK074868NIDDK NIH HHS P30 DK063491NIDDK NIH HHS R01 DK033651NIDDK NIH HHS R37 DK033651NIDDK NIH HHS T32 DK007494
6 · The paper itself

Abstract

Insulin resistance, tissue inflammation, and adipose tissue dysfunction are features of obesity and Type 2 diabetes. We generated adipocyte-specific Nuclear Receptor Corepressor (NCoR) knockout (AKO) mice to investigate the function of NCoR in adipocyte biology, glucose and insulin homeostasis. Despite increased obesity, glucose tolerance was improved in AKO mice, and clamp studies demonstrated enhanced insulin sensitivity in liver, muscle, and fat. Adipose tissue macrophage infiltration and inflammation were also decreased. PPARγ response genes were upregulated in adipose tissue from AKO mice and CDK5-mediated PPARγ ser-273 phosphorylation was reduced, creating a constitutively active PPARγ state. This identifies NCoR as an adaptor protein that enhances the ability of CDK5 to associate with and phosphorylate PPARγ. The dominant function of adipocyte NCoR is to transrepress PPARγ and promote PPARγ ser-273 phosphorylation, such that NCoR deletion leads to adipogenesis, reduced inflammation, and enhanced systemic insulin sensitivity, phenocopying the TZD-treated state.

Indexed as

Insulin ResistanceAdipocytesAnimalsCo-Repressor ProteinsDiabetes Mellitus, Type 2Diet, High-FatMaleMiceMice, Inbred C57BLMice, KnockoutNuclear Receptor Co-Repressor 1PhosphorylationPPAR gammaThiazolidinedionesCo-Repressor ProteinsNcor1 protein, mouseNuclear Receptor Co-Repressor 1PPAR gammaThiazolidinediones

Identifiers

PMID22078880
PMCPMC3783197
OpenAlexW2123774383

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.