Evidence map›Paper›PMID 23307192›Full record

ReviewCurrent diabetes reports2013

Epigenetics of insulin resistance: an emerging field in translational medicine.

Silvia Sookoian, Carlos J Pirola

Abstract readReview
PubMed Publisher
In one paragraph

Review in Current diabetes reports, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
–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

9 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
  4. Insulin Sensitivity Is Associated with Lipoprotein Lipase (International journal of molecular sciences · 2019
    Article
  5. Review
  6. Review
  7. Metabolic syndrome in children (Review).Experimental and therapeutic medicine · 2016
    Article
  8. Article
  9. Review
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.

Silvia SookoianDepartment of Clinical and Molecular Hepatology, Institute of Medical Research A Lanari-IDIM, University of Buenos Aires-National Council of Scientific and Technological Research (CONICET), Ciudad Autónoma de Buenos Aires, Argentina. sookoian.silvia@lanari.fmed.uba.ar
Carlos J Pirola

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In this article, we review the current knowledge of and recent insights into the role of epigenetic factors in the development of insulin resistance (IR), with emphasis on peroxisome proliferator-activated receptor gamma coactivator 1α (PPARGC1A or PGC1α) methylation on fetal programming and liver modulation of glucose-related phenotypes. We discuss the pathogenesis of IR beyond the integrity of β-cell function and illustrate the novel concept of mitochondrial epigenetics to explain the pathobiology of metabolic-syndrome-related phenotypes. Moreover, we discuss whether epigenetic marks in genes of the circadian rhythm system are able to modulate insulin/glucose-related metabolic functions and place hypoxia inducible factor 1 α (HIF1α) as a part of the master CLOCK gene/protein interaction network that might modulate IR. Finally, we highlight relevant information about epigenetic marks and IR so that clinicians practicing in the community may envision future areas of medical intervention and predict putative biomarkers for early disease detection.

Indexed as

DNA MethylationEpigenomicsHeat-Shock ProteinsHumansInsulin ResistancePeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaTranscription FactorsTranslational Research, BiomedicalHeat-Shock ProteinsPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaPPARGC1A protein, humanTranscription Factors

Identifiers

What OpenQuestion holds

Textmetadata
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.