Evidence map›Paper›PMID 21414768›Full record

ArticleThe Journal of nutritional biochemistry2012

Acute and chronic saturated fatty acid treatment as a key instigator of the TLR-mediated inflammatory response in human adipose tissue, in vitro.

Elham M Youssef-Elabd, Kirsty C McGee, Gyanendra Tripathi, Nasser Aldaghri, Mohga S Abdalla, Hayat M Sharada, Esmat Ashour, Ashraf I Amin, Antonio Ceriello, Joseph P O'Hare and 3 more

Open access · greenAbstract read
In one paragraph

Article in The Journal of nutritional biochemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

28 citing papers in PubMed, 70 citations in OpenAlex.

  1. Trial
  2. Review
  3. Article
  4. Article
  5. Review
  6. Article
  7. Asthma and obesity: endotoxin another insult to add to injury?Clinical science (London, England : 1979) · 2021
    Review
  8. Review
  9. Article
  10. Article
  11. Review
  12. The Exercise Training Modulatory Effects on the Obesity-Induced Immunometabolic Dysfunctions.Diabetes, metabolic syndrome and obesity : targets and therapy · 2020
    Review
  13. Review
  14. Macronutrients and the Adipose-Liver Axis in Obesity and Fatty Liver.Cellular and molecular gastroenterology and hepatology · 2019
    Review
  15. Article
  16. Review
  17. The Effect and Mechanism of KLF7 in the TLR4/NF-Mediators of inflammation · 2018
    Article
  18. Review
  19. Nutrients and Oxidative Stress: Friend or Foe?Oxidative medicine and cellular longevity · 2018
    Review
  20. 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

13 authors at 5 institutions in 4 countries.

Elham M Youssef-ElabdBiochemistry Department, National Research Centre, Dokki, Giza, Egypt 12622.
Kirsty C McGee
Gyanendra Tripathi
Nasser Aldaghri
Mohga S Abdalla
Hayat M Sharada
Esmat Ashour
Ashraf I Amin
Antonio Ceriello
Joseph P O'Hare
Sudhesh Kumar
Philip G McTernan
Alison L Harte
University of Warwick · GBHelwan University · EGNational Research Centre · EGConsorci Institut D'Investigacions Biomediques August Pi I Sunyer · ESKing Saud University · SA

Funding

British Heart FoundationMedical Research Council
6 · The paper itself

Abstract

A post-prandial increase in saturated fatty acids (SFAs) and glucose (Glc) activates an inflammatory response, which may be prolonged following restoration of physiological SFAs and Glc levels--a finding referred to as 'metabolic memory'. This study examined chronic and oscillating SFAs and Glc on the inflammatory signalling pathway in human adipose tissue (AT) and adipocytes (Ads) and determined whether Ads are subject to "metabolic memory." Abdominal (Abd) subcutaneous (Sc) explants and Ads were treated with chronic low glucose (L-Glc): 5.6 mM and high glucose (H-Glc): 17.5 mM, with low (0.2 mM) and high (2 mM) SFA for 48 h. Abd Sc explants and Ads were also exposed to the aforementioned treatment regimen for 12-h periods, with alternating rest periods of 12 h in L-Glc. Chronic treatment with L-Glc and high SFAs, H-Glc and high SFAs up-regulated key factors of the nuclear factor-κB (NFκB) pathway in Abd Sc AT and Ads (TLR4, NFκB; P<.05), whilst down-regulating MyD88. Oscillating Glc and SFA concentrations increased TLR4, NFκB, IKKβ (P<.05) in explants and Ads and up-regulated MyD88 expression (P<.05). Both tumor necrosis factor α and interleukin 6 (P<.05) secretion were markedly increased in chronically treated Abd Sc explants and Ads whilst, with oscillating treatments, a sustained inflammatory effect was noted in absence of treatment. Therefore, SFAs may act as key instigators of the inflammatory response in human AT via NFκB activation, which suggests that short-term exposure of cells to uncontrolled levels of SFAs and Glc leads to a longer-term inflammatory insult within the Ad, which may have important implications for patients with obesity and Type 2 diabetes.

Indexed as

AdipocytesAdipose TissueAdultFatty AcidsFemaleGlucoseHumansI-kappa B KinaseInflammationInterleukin-6In Vitro TechniquesMiddle AgedMitogen-Activated Protein Kinase 8Mitogen-Activated Protein Kinase 9Myeloid Differentiation Factor 88NF-kappa BFatty AcidsGlucoseI-kappa B KinaseInterleukin-6Mitogen-Activated Protein Kinase 8Mitogen-Activated Protein Kinase 9MYD88 protein, humanMyeloid Differentiation Factor 88NF-kappa BTLR4 protein, humanTNF Receptor-Associated Factor 6Toll-Like Receptor 4Tumor Necrosis Factor-alpha

Identifiers

PMID21414768
PMCPMC3243902
OpenAlexW2102373269

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.