Evidence map›Paper›PMID 24962583›Full record

ArticleThe Journal of biological chemistry2014

Relationship between a common variant in the fatty acid desaturase (FADS) cluster and eicosanoid generation in humans.

Austin G Hester, Robert C Murphy, Charis J Uhlson, Priscilla Ivester, Tammy C Lee, Susan Sergeant, Leslie R Miller, Timothy D Howard, Rasika A Mathias, Floyd H Chilton

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing 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

47 citing papers in PubMed, 73 citations in OpenAlex.

  1. Trial
  2. Trial
  3. Trial
  4. Trial
  5. Fatty acid desaturase genetic variations in heart failure and cardiovascular disease.American heart journal plus : cardiology research and practice · 2025
    Review
  6. Article
  7. The influence ofFrontiers in nutrition · 2025
    Article
  8. Observational
  9. Hepatocyte-SpecificInternational journal of molecular sciences · 2024
    Article
  10. Article
  11. Inhaled toxicants and pulmonary lipid metabolism: biological consequences and therapeutic interventions.Toxicological sciences : an official journal of the Society of Toxicology · 2023
    Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Review
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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

10 authors at 3 institutions in 1 country.

Austin G HesterFrom the Department of Urology, Wake Forest University School of Medicine, Winston-Salem, North Carolina 27157, the Department of Physiology/Pharmacology, Wake Forest University School of Medicine, Winston-Salem, North Carolina 27157.
Robert C Murphythe Department of Pharmacology, University of Colorado Denver, Aurora, Colorado 80045.
Charis J Uhlsonthe Department of Pharmacology, University of Colorado Denver, Aurora, Colorado 80045.
Priscilla Ivesterthe Department of Physiology/Pharmacology, Wake Forest University School of Medicine, Winston-Salem, North Carolina 27157, the Center for Botanical Lipids and Inflammatory Disease Prevention, Wake Forest University School of Medicine, Winston-Salem, North Carolina 27157.
Tammy C Leethe Department of Physiology/Pharmacology, Wake Forest University School of Medicine, Winston-Salem, North Carolina 27157, the Center for Botanical Lipids and Inflammatory Disease Prevention, Wake Forest University School of Medicine, Winston-Salem, North Carolina 27157.
Susan Sergeantthe Center for Botanical Lipids and Inflammatory Disease Prevention, Wake Forest University School of Medicine, Winston-Salem, North Carolina 27157, the Department of Biochemistry, Wake Forest University School of Medicine, Winston-Salem, North Carolina 27157.
Leslie R Millerthe Department of Physiology/Pharmacology, Wake Forest University School of Medicine, Winston-Salem, North Carolina 27157.
Timothy D Howardthe Center for Human Genomics, Wake Forest University School of Medicine, Winston-Salem, North Carolina 27157.
Rasika A Mathiasthe Division of Allergy and Clinical Immunology, Department of Medicine, The Johns Hopkins University, Baltimore, Maryland 21224, and.
Floyd H Chiltonthe Department of Physiology/Pharmacology, Wake Forest University School of Medicine, Winston-Salem, North Carolina 27157, the Center for Botanical Lipids and Inflammatory Disease Prevention, Wake Forest University School of Medicine, Winston-Salem, North Carolina 27157, the Molecular Medicine and Translation Sciences, Wake Forest University School of Medicine, Winston-Salem, North Carolina 27157 schilton@wakehealth.edu.
Wake Forest University · USUniversity of Colorado Denver · USJohns Hopkins University · US

Funding

Wake Forest Clinical and Translational Science AwardUL1TR001420 · NCATS · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI ARD, JAMY D, FOLEY, KRISTIE L · 2015 to 2023
$32.3M
The Wake Forest Center for Botanical Lipids and Inflammatory Disease PreventionP50AT002782 · NCCIH · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI CHILTON, FLOYD H · 2005 to 2014
$15.3M
NCATS NIH HHS UL1 TR001420NCCIH NIH HHS P50 AT002782
6 · The paper itself

Abstract

Dramatic shifts in the Western diet have led to a marked increase in the dietary intake of the n-6 polyunsaturated fatty acid (PUFA), linoleic acid (LA). Dietary LA can then be converted to arachidonic acid (ARA) utilizing three enzymatic steps. Two of these steps are encoded for by the fatty acid desaturase (FADS) cluster (chromosome 11, 11q12.2-q13) and certain genetic variants within the cluster are highly associated with ARA levels. However, no study to date has examined whether these variants further influence pro-inflammatory, cyclooxygenase and lipoxygenase eicosanoid products. This study examined the impact of a highly influential FADS SNP, rs174537 on leukotriene, HETE, prostaglandin, and thromboxane biosynthesis in stimulated whole blood. Thirty subjects were genotyped at rs174537 (GG, n = 11; GT, n = 13; TT, n = 6), a panel of fatty acids from whole serum was analyzed, and precursor-to-product PUFA ratios were calculated as a marker of the capacity of tissues (particularly the liver) to synthesize long chain PUFAs. Eicosanoids produced by stimulated human blood were measured by LC-MS/MS. We observed an association between rs174537 and the ratio of ARA/LA, leukotriene B4, and 5-HETE but no effect on levels of cyclooxygenase products. Our results suggest that variation at rs174537 not only impacts the synthesis of ARA but the overall capacity of whole blood to synthesize 5-lipoxygenase products; these genotype-related changes in eicosanoid levels could have important implications in a variety of inflammatory diseases.

Indexed as

Polymorphism, Single NucleotideAdultArachidonic AcidDelta-5 Fatty Acid DesaturaseDiet, WesternEicosanoidsFatty Acid DesaturasesFemaleHumansInflammationInflammation MediatorsLeukotriene B4Linoleic AcidMetabolic Networks and PathwaysMiddle AgedMultigene FamilyArachidonic AcidDelta-5 Fatty Acid DesaturaseEicosanoidsFADS2 protein, humanFatty Acid DesaturasesInflammation MediatorsLeukotriene B4Linoleic AcidArachidonic Acid (AA) (ARA)EicosanoidFatty Acid DesaturaseInflammationNutritionPolyunsaturated Fatty Acid (PUFA)Single-nucleotide Polymorphism (SNP)

Identifiers

PMID24962583
PMCPMC4139254
OpenAlexW2047155548

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.