Evidence map›Paper›PMID 24086512›Full record

ArticlePloS one2013

Proteomics analysis of human obesity reveals the epigenetic factor HDAC4 as a potential target for obesity.

Mohamed Abu-Farha, Ali Tiss, Jehad Abubaker, Abdelkrim Khadir, Fahad Al-Ghimlas, Irina Al-Khairi, Engin Baturcam, Preethi Cherian, Naser Elkum, Maha Hammad and 6 more

Open access · goldAbstract readComparative Study
In one paragraph

Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed, 1 pooled it
4.2field-weighted citation impact, top 5% 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

49 citing papers in PubMed, 1 synthesis or guideline pooled it, 87 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Trial
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Review
  10. Article
  11. Review
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Review
  18. CD47 and thrombospondin-1 regulation of mitochondria, metabolism, and diabetes.American journal of physiology. Cell physiology · 2021
    Review
  19. Thrombospondin 1 in Metabolic Diseases.Frontiers in endocrinology · 2021
    Review
  20. 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

16 authors at 2 institutions in 2 countries.

Mohamed Abu-FarhaDepartment of Biomedical Research, Dasman Diabetes Institute, Kuwait, Kuwait.
Ali Tiss
Jehad Abubaker
Abdelkrim Khadir
Fahad Al-Ghimlas
Irina Al-Khairi
Engin Baturcam
Preethi Cherian
Naser Elkum
Maha Hammad
Jeena John
Sina Kavalakatt
Samia Warsame
Kazem Behbehani
Said Dermime
Mohammed Dehbi
Dasman Diabetes Institute · KWKing Fahad Specialist Hospital · SA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Sedentary lifestyle and excessive energy intake are prominent contributors to obesity; a major risk factors for the development of insulin resistance, type 2 diabetes and cardiovascular diseases. Elucidating the molecular mechanisms underlying these chronic conditions is of relevant importance as it might lead to the identification of novel anti-obesity targets. The purpose of the current study is to investigate differentially expressed proteins between lean and obese subjects through a shot-gun quantitative proteomics approach using peripheral blood mononuclear cells (PBMCs) extracts as well as potential modulation of those proteins by physical exercise. Using this approach, a total of 47 proteins showed at least 1.5 fold change between lean and obese subjects. In obese, the proteomic profiling before and after 3 months of physical exercise showed differential expression of 38 proteins. Thrombospondin 1 (TSP1) was among the proteins that were upregulated in obese subjects and then decreased by physical exercise. Conversely, the histone deacetylase 4 (HDAC4) was downregulated in obese subjects and then induced by physical exercise. The proteomic data was further validated by qRT-PCR, Western blot and immunohistochemistry in both PBMCs and adipose tissue. We also showed that HDAC4 levels correlated positively with maximum oxygen consumption (VO2 Max) but negatively with body mass index, percent body fat, and the inflammatory chemokine RANTES. In functional assays, our data indicated that ectopic expression of HDAC4 significantly impaired TNF-α-dependent activation of NF-κB, establishing thus a link between HDAC4 and regulation of the immune system. Together, the expression pattern of HDAC4 in obese subjects before and after physical exercise, its correlation with various physical, clinical and metabolic parameters along with its inhibitory effect on NF-κB are suggestive of a protective role of HDAC4 against obesity. HDAC4 could therefore represent a potential therapeutic target for the control and management of obesity and presumably insulin resistance.

Indexed as

Adipose TissueBlotting, WesternBody CompositionBody Mass IndexChemokine CCL5Epigenesis, GeneticExerciseGene Expression ProfilingGene Expression RegulationHistone DeacetylasesHumansImmunohistochemistryLeukocytes, MononuclearObesityOxygen ConsumptionProteomicsCCL5 protein, humanChemokine CCL5HDAC4 protein, humanHistone DeacetylasesRepressor ProteinsThrombospondin 1

Identifiers

PMID24086512
PMCPMC3782461
OpenAlexW1979729557

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.