Evidence map›Paper›PMID 22504298›Full record

ReviewBiochimica et biophysica acta2012

Controlling a master switch of adipocyte development and insulin sensitivity: covalent modifications of PPARγ.

Z Elizabeth Floyd, Jacqueline M Stephens

Open access · greenAbstract readReview
In one paragraph

Review in Biochimica et biophysica acta, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed
4.7field-weighted citation impact, top 4% 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

48 citing papers in PubMed, 82 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Review
  10. Common Variation inFrontiers in cardiovascular medicine · 2022
    Article
  11. Review
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. The PPARPPAR research · 2020
    Review
  19. Review
  20. Cardiac myocyte KLF5 regulates body weight via alteration of cardiac FGF21.Biochimica et biophysica acta. Molecular basis of disease · 2019
    Article
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

2 authors at 1 institution in 1 country.

Z Elizabeth FloydUbiquitin Biology Laboratory, Pennington Biomedical Research Resaerch Center, Louisiana Sate University Systems, Baton Rouge, LA 70808, USA.
Jacqueline M Stephens
Pennington Biomedical Research Center · US

Funding

Regulation of PPARgamma in Adipocytes by Siah2R56DK089020 · NIDDK · LSU PENNINGTON BIOMEDICAL RESEARCH CTR · PI FLOYD, ZELPHA ELIZABETH · 2010 to 2011
$442k
NIDDK NIH HHS R56 DK089020NIDDK NIH HHS R56DK089020
6 · The paper itself

Abstract

Adipocytes are highly specialized cells that play a central role in lipid homeostasis and the maintenance of energy balance. Obesity, an excessive accumulation of adipose tissue, is a major risk factor for the development of Type 2 diabetes mellitus (T2DM), cardiovascular disease, and hypertension. A variety of studies suggest that obesity and T2DM can be linked to a breakdown in the regulatory mechanisms that control the expression and transcriptional activity of PPARγ. PPARγ is a nuclear hormone receptor that functions as a master switch in controlling adipocyte differentiation and development. Also important in controlling glucose homeostasis and insulin sensitivity, PPARγ is a ligand-dependent transcription factor that is the functional receptor for the anti-diabetic thiazolidinediones (TZDs). In the last fifteen years, a variety of covalent modifications of PPARγ activity have been identified and studied. These covalent modifications include phosphorylation, ubiquitylation, O-GlcNAcylation and SUMOylation. Covalent modifications of PPARγ represent key regulatory mechanisms that control both PPARγ protein stability and transcriptional activity. A variety of PPARγ transgenic models, including mice heterozygous for PPARγ, have demonstrated the importance of PPARγ expression in glucose homeostasis and insulin resistance. In the following review, we have highlighted the regulation of PPARγ by covalent modifications, the interplay between these interactions and how these post-translational modifications impact metabolic disease states.

Indexed as

AcylationAdipocytesAdipose TissueAnimalsBlood GlucoseCardiovascular DiseasesCyclin-Dependent Kinase 5Diabetes Mellitus, Type 2Fibroblast Growth FactorsHomeostasisHumansHypoglycemic AgentsInsulinInsulin ResistanceLigandsMiceBlood GlucoseCyclin-Dependent Kinase 5fibroblast growth factor 21Fibroblast Growth FactorsHypoglycemic AgentsInsulinLigandsPPAR gammaSmall Ubiquitin-Related Modifier ProteinsThiazolidinediones

Identifiers

PMID22504298
PMCPMC3355475
OpenAlexW2101676867

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.