Evidence map›Paper›PMID 24859760›Full record

ArticleJournal of lipid research2014

Abnormal n-6 fatty acid metabolism in cystic fibrosis is caused by activation of AMP-activated protein kinase.

Obi C Umunakwe, Adam C Seegmiller

Open access · hybridAbstract read
In one paragraph

Article in Journal of lipid research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.0field-weighted citation impact, top 21% 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

14 citing papers in PubMed, 18 citations in OpenAlex.

  1. Review
  2. Reduced Sphingosine in Cystic Fibrosis Increases Susceptibility toInternational journal of molecular sciences · 2023
    Article
  3. Article
  4. Article
  5. Review
  6. Article
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  8. Article
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  11. Article
  12. Impact of estrogens and estrogen receptor-α in brain lipid metabolism.American journal of physiology. Endocrinology and metabolism · 2018
    Review
  13. Article
  14. 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

2 authors at 1 institution in 1 country.

Obi C UmunakweDepartment of Pathology, Microbiology, and Immunology, Vanderbilt University School of Medicine, Nashville, TN.
Adam C SeegmillerDepartment of Pathology, Microbiology, and Immunology, Vanderbilt University School of Medicine, Nashville, TN.
Vanderbilt University · US

Funding

MEDICAL SCIENTIST TRAINING PROGRAMT32GM007347 · NIGMS · VANDERBILT UNIVERSITY · PI WILLIAMS, CHRISTOPHER S. · 1985 to 2023
$26.3M
Defining a mechanism for altered PUFA metabolism in cystic fibrosisF30DK097872 · NIDDK · VANDERBILT UNIVERSITY · PI UMUNAKWE, OBINNA · 2013 to 2015
$116k
NIDDK NIH HHS F30 DK097872NIGMS NIH HHS T32 GM007347
6 · The paper itself

Abstract

Cystic fibrosis (CF) patients and model systems exhibit consistent abnormalities in PUFA metabolism, including increased metabolism of linoleate to arachidonate. Recent studies have connected these abnormalities to increased expression and activity of the Δ6- and Δ5-desaturase enzymes. However, the mechanism connecting these changes to the CF transmembrane conductance regulator (CFTR) mutations responsible for CF is unknown. This study tests the hypothesis that increased activity of AMP-activated protein kinase (AMPK), previously described in CF bronchial epithelial cells, causes these changes in fatty acid metabolism by driving desaturase expression. Using CF bronchial epithelial cell culture models, we confirm elevated activity of AMPK in CF cells and show that it is due to increased phosphorylation of AMPK by Ca(2+)/calmodulin-dependent protein kinase kinase β (CaMKKβ). We also show that inhibition of AMPK or CaMKKβ reduces desaturase expression and reverses the metabolic alterations seen in CF cells. These results signify a novel AMPK-dependent mechanism linking the genetic defect in CF to alterations in PUFA metabolism.

Indexed as

AMP-Activated Protein KinasesCalcium-Calmodulin-Dependent Protein Kinase KinaseCell LineCystic FibrosisCystic Fibrosis Transmembrane Conductance RegulatorEpithelial CellsFatty Acids, Omega-6HumansRespiratory MucosaAMP-Activated Protein KinasesCalcium-Calmodulin-Dependent Protein Kinase KinaseCFTR protein, humanCystic Fibrosis Transmembrane Conductance RegulatorFatty Acids, Omega-6adenosine 5′-monophosphate-activated protein kinasearachidonic acidfatty acid desaturaselinoleic acidpolyunsaturated fatty acid

Identifiers

PMID24859760
PMCPMC4076094
OpenAlexW2163695227

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.