Evidence map›Paper›PMID 31883537›Full record

ArticleLipids in health and disease2019

Oleic acid influences the adipogenesis of 3T3-L1 cells via DNA Methylation and may predispose to obesity and obesity-related disorders.

Malgorzata Malodobra-Mazur, Aneta Cierzniak, Tadeusz Dobosz

Open access · goldAbstract read
In one paragraph

Article in Lipids in health and disease, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed
4.6field-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, 71 citations in OpenAlex.

  1. Trial
  2. Undernutrition-related diabetes in mice is linked to early undernutrition.American journal of physiology. Endocrinology and metabolism · 2026
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  7. Response of Primary Human Adipocytes to Fatty Acid Treatment.Journal of cellular and molecular medicine · 2025
    Article
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  18. Epigenetic Regulation in Lean Nonalcoholic Fatty Liver Disease.International journal of molecular sciences · 2023
    Review
  19. Article
  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

3 authors at 1 institution in 1 country.

Malgorzata Malodobra-MazurDepartment of Forensic Medicine, Molecular Techniques Unit, Wroclaw Medical University, Sklodowskiej-Curie 52, 50-369, Wroclaw, Poland. malgorzata.malodobra-mazur@umed.wroc.pl.ORCID http://orcid.org/0000-0002-9864-5928
Aneta CierzniakDepartment of Forensic Medicine, Molecular Techniques Unit, Wroclaw Medical University, Sklodowskiej-Curie 52, 50-369, Wroclaw, Poland.
Tadeusz DoboszDepartment of Forensic Medicine, Molecular Techniques Unit, Wroclaw Medical University, Sklodowskiej-Curie 52, 50-369, Wroclaw, Poland.
Wroclaw Medical University · PL

Funding

Nutricia Foundation RG3/2016
6 · The paper itself

Abstract

backgroundAdipogenesis is the process of adipocytes formation from unspecialized progenitor cells called mesenchymal stromal cells. Numerous mechanisms including epigenetic regulation modulate the correct progress of this process. Dietary exposures occurring over a specific period of time might cause long-lasting and even permanent changes in gene expression regulated by epigenetic mechanisms. For that reason, we investigated the adipogenesis of 3 T3-L1 cells with the excess of saturated and monounsaturated fatty acids and their influence on global and site-specific DNA methylation in these cells. MATERIALS AND

methods3T3-L1 cells were cultured in vitro to obtain 100% of confluence, then the adipogenesis was induced by a differentiation cocktail with the addition of the excess of 0.25 mM and 0.5 mM of palmitic (16:0), stearic (18:0) and oleic (18:1n-9) acids. DNA and RNA were extracted at five-time points to assess the adipogenesis process. The phenotype of mature adipocytes (insulin sensitivity, adipokines secretion, fat content) was estimated in fully mature adipocytes. DNA methylation was investigated both during adipogenesis and in mature adipocytes.

resultsOleic acids stimulated expression of C/ebpα and Pparγ, which was correlated with lower methylation levels at promoters sites. Furthermore, cells cultured with an excess of oleic acid were characterized by higher lipid accumulation rate, higher leptin, and lower adiponectin secretion. Moreover, in all experimental cells, insulin signaling and glucose utilization were impaired.

conclusionOleic acid affected the methylation of Pparγ and C/ebpα promoters, what correlated with higher expression. Furthermore, examined free fatty acids influenced the phenotype of mature adipocytes, especially insulin signaling pathway and adipokine secretion.

Indexed as

3T3-L1 CellsAdipocytesAdipogenesisAdipokinesAnimalsCCAAT-Enhancer-Binding ProteinsCell DifferentiationDisease Models, AnimalDNA MethylationEpigenesis, GeneticGlucoseHumansInsulinInsulin ResistanceLipid MetabolismMesenchymal Stem CellsAdipokinesCCAAT-Enhancer-Binding ProteinsCEBPA protein, mouseGlucoseInsulinOleic AcidPPAR gammaPparg protein, mouse3T3-L1AdipogenesisDNA methylationInsulin signalingOleic acidPalmitic acidStearic acid

Identifiers

PMID31883537
PMCPMC6935146
OpenAlexW2998299632

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Registered trials

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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.