Evidence map›Paper›PMID 22535284›Full record

ArticleJournal of physiology and biochemistry2012

Effects of hyperoxia exposure on metabolic markers and gene expression in 3T3-L1 adipocytes.

P Quintero, P González-Muniesa, D F García-Díaz, J A Martínez

Abstract read
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In one paragraph

Article in Journal of physiology and biochemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing 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

19 citing papers in PubMed.

  1. Review
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  3. Article
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  6. Dual role of ANGPTL4 in inflammation.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2023
    Review
  7. Article
  8. Role of adipose tissue macrophages in obesity-related disorders.The Journal of experimental medicine · 2022
    Article
  9. Article
  10. Constitutive transgenic α-Klotho overexpression enhances resilience to and recovery from murine acute lung injury.American journal of physiology. Lung cellular and molecular physiology · 2021
    Article
  11. Article
  12. Article
  13. Adapting to obesity with adipose tissue inflammation.Nature reviews. Endocrinology · 2017
    Review
  14. Article
  15. Review
  16. Review
  17. Article
  18. Review
  19. 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

4 authors.

P QuinteroDepartment of Nutrition, Food Science, Physiology and Toxicology, University of Navarra, c/Irunlarrea 1, 31008 Pamplona, Spain.
P González-Muniesa
D F García-Díaz
J A Martínez

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Adipose tissue often becomes poorly oxygenated in obese subjects. This feature may provide cellular mechanisms involving chronic inflammation processes such as the release of pro-inflammatory cytokines and macrophage infiltration. In this context, the purpose of the present study was to determine whether a hyperoxia exposure on mature adipocytes may influence the expression of some adipokines and involve favorable changes in specific metabolic variables. Thus, 3T3-L1 adipocytes (14 days differentiated) were treated with 95 % oxygen for 24 h. Cell viability, intra and extracellular reactive oxygen species (ROS) content, glucose uptake, as well as lactate and glycerol concentrations were measured in the culture media. Also, mRNA levels of hypoxia-inducible factor (HIF)-1α, leptin, interleukin (IL)-6, monocyte chemotactic protein (MCP)-1, peroxisome proliferator-activated receptor (PPAR)-γ, adiponectin, and angiopoietin-related protein (ANGPTL)4 were analyzed. Hyperoxia treatment increased intra and extracellular ROS content, reduced glucose uptake and lactate release and increased glycerol release. Additionally, a higher oxygen tension led to an upregulation of the expression of IL-6, MCP-1, and PPAR-γ, while ANGPTL4 was downregulated in the hyperoxia group with respect to control. The present data shows that hyperoxia treatment seems to produce an inflammatory response due to the release of ROS and the upregulation of pro-inflammatory adipokines, such as IL-6 and MCP-1. On the other hand, hyperoxia may have an indirect effect on insulin sensitivity due to the upregulation of PPAR-γ signaling as well as a possible modulation of both glucose and lipid metabolic markers. To our knowledge, this is the first study analyzing the effect of hyperoxia in 3T3-L1 adipocytes.

Indexed as

Gene Expression3T3-L1 CellsAdipocytesAnimalsBiomarkersCell HypoxiaCell SurvivalChemokine CCL2Culture MediaGlucoseHypoxia-Inducible Factor 1, alpha SubunitInflammation MediatorsInterleukin-6Lactic AcidMiceObesityBiomarkersChemokine CCL2Culture MediaGlucoseHif1a protein, mouseHypoxia-Inducible Factor 1, alpha SubunitInflammation MediatorsInterleukin-6interleukin-6, mouseLactic AcidReactive Oxygen Species

Identifiers

What OpenQuestion holds

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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.