Evidence map›Paper›PMID 33809964›Full record

ArticleMetabolites2021

Stable Isotopic Tracer Phospholipidomics Reveals Contributions of Key Phospholipid Biosynthetic Pathways to Low Hepatocyte Phosphatidylcholine to Phosphatidylethanolamine Ratio Induced by Free Fatty Acids.

Kang-Yu Peng, Christopher K Barlow, Helene Kammoun, Natalie A Mellett, Jacquelyn M Weir, Andrew J Murphy, Mark A Febbraio, Peter J Meikle

Open access · goldAbstract read
In one paragraph

Article in Metabolites, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.9field-weighted citation impact, top 26% 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

8 citing papers in PubMed, 11 citations in OpenAlex.

  1. Review
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  4. Current neuroprotective agents in stroke.Turkish journal of physical medicine and rehabilitation · 2024
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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

8 authors at 2 institutions in 1 country.

Kang-Yu PengMetabolomics Laboratory, Baker Heart and Diabetes Institute, Melbourne, VIC 3004, Australia.ORCID 0000-0003-4024-4088
Christopher K BarlowMetabolomics Laboratory, Baker Heart and Diabetes Institute, Melbourne, VIC 3004, Australia.
Helene KammounHematopoiesis & Leukocyte Biology Laboratory, Baker Heart and Diabetes Institute, Melbourne, VIC 3004, Australia.
Natalie A MellettMetabolomics Laboratory, Baker Heart and Diabetes Institute, Melbourne, VIC 3004, Australia.
Jacquelyn M WeirMetabolomics Laboratory, Baker Heart and Diabetes Institute, Melbourne, VIC 3004, Australia.
Andrew J MurphyHematopoiesis & Leukocyte Biology Laboratory, Baker Heart and Diabetes Institute, Melbourne, VIC 3004, Australia.
Mark A FebbraioCellular & Molecular Metabolism Laboratory, Drug Discovery Biology, Monash Institute of Pharmaceutical Sciences, Monash University, Melbourne, VIC 3052, Australia.
Peter J MeikleMetabolomics Laboratory, Baker Heart and Diabetes Institute, Melbourne, VIC 3004, Australia.ORCID 0000-0002-2593-4665
Baker Heart and Diabetes Institute · AUMonash University · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

There is a strong association between hepatocyte phospholipid homeostasis and non-alcoholic fatty liver disease (NAFLD). The phosphatidylcholine to phosphatidylethanolamine ratio (PC/PE) often draws special attention as genetic and dietary disruptions to this ratio can provoke steatohepatitis and other signs of NAFLD. Here we demonstrated that excessive free fatty acid (1:2 mixture of palmitic and oleic acid) alone was able to significantly lower the phosphatidylcholine to phosphatidylethanolamine ratio, along with substantial alterations to phospholipid composition in rat hepatocytes. This involved both a decrease in hepatocyte phosphatidylcholine (less prominent) and an increase in phosphatidylethanolamine, with the latter contributing more to the lowered ratio. Stable isotopic tracer phospholipidomic analysis revealed several previously unidentified changes that were triggered by excessive free fatty acid. Importantly, the enhanced cytidine diphosphate (CDP)-ethanolamine pathway activity appeared to be driven by the increased supply of preferred fatty acid substrates. By contrast, the phosphatidylethanolamine

Indexed as

CDP-choline pathwayCDP-ethanolamine pathwayflux analysisfree fatty acidlipidomicsphosphatidylethanolamine N-methyl transferase (PEMT) pathwaysteatosis

Identifiers

PMID33809964
PMCPMC8004269
OpenAlexW3136411521

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.