Evidence map›Paper›PMID 24714086›Full record

ArticleInternational journal of molecular sciences2014

Fatty acid elongation in non-alcoholic steatohepatitis and hepatocellular carcinoma.

Sonja M Kessler, Yvette Simon, Katja Gemperlein, Kathrin Gianmoena, Cristina Cadenas, Vincent Zimmer, Juliane Pokorny, Ahmad Barghash, Volkhard Helms, Nico van Rooijen and 6 more

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
4.7field-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

31 citing papers in PubMed, 47 citations in OpenAlex.

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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

16 authors at 6 institutions in 3 countries.

Sonja M KesslerDepartment of Pharmacy, Pharmaceutical Biology, Saarland University, Campus C2 2, 66123 Saarbrücken, Germany. s.kessler@mx.uni-saarland.de.
Yvette SimonDepartment of Pharmacy, Pharmaceutical Biology, Saarland University, Campus C2 2, 66123 Saarbrücken, Germany. yvette.simon84@gmail.com.
Katja GemperleinDepartment of Pharmacy, Pharmaceutical Biotechnology, Saarland University and Helmholtz Institute for Pharmaceutical Research Saarland (HIPS), Helmholtz Centre for Infection Research (HZI), 66123 Saarbrücken, Germany. Katja.Gemperlein@helmholtz-hzi.de.
Kathrin GianmoenaSystems Toxicology, Leibniz Research Centre for Working Environment and Human Factors (IfADo) at the TU Dortmund, Ardeystr. 67, 44139 Dortmund, Germany. gianmoena@ifado.de.
Cristina CadenasSystems Toxicology, Leibniz Research Centre for Working Environment and Human Factors (IfADo) at the TU Dortmund, Ardeystr. 67, 44139 Dortmund, Germany. cadenas@ifado.de.
Vincent ZimmerDepartment of Medicine II, Saarland University Medical Center, Kirrberger Str., 66421 Homburg, Germany. Vincent.Zimmer@uniklinikum-saarland.de.
Juliane PokornyInstitute of Pathology, Saarland University, Kirrberger Str., 66421 Homburg, Germany. juliane.pokorny@uniklinikum-saarland.de.
Ahmad BarghashCenter for Bioinformatics, Saarland University, Campus E2 1, 66123 Saarbrücken, Germany. barghash@bioinformatik.uni-saarland.de.
Volkhard HelmsCenter for Bioinformatics, Saarland University, Campus E2 1, 66123 Saarbrücken, Germany. volkhard.helms@bioinformatik.uni-saarland.de.
Nico van RooijenDepartment of Molecular Cell Biology, Faculty of Medicine, Vrije Universiteit, Van der Boechorststraat 7, 1081 BT Amsterdam, The Netherlands. nvanrooijen@clodronateliposomes.org.
Rainer M BohleInstitute of Pathology, Saarland University, Kirrberger Str., 66421 Homburg, Germany. rainer.bohle@uniklinikum-saarland.de.
Frank LammertDepartment of Medicine II, Saarland University Medical Center, Kirrberger Str., 66421 Homburg, Germany. Frank.Lammert@uniklinikum-saarland.de.
Jan G HengstlerSystems Toxicology, Leibniz Research Centre for Working Environment and Human Factors (IfADo) at the TU Dortmund, Ardeystr. 67, 44139 Dortmund, Germany. hengstler@ifado.de.
Rolf MuellerDepartment of Pharmacy, Pharmaceutical Biotechnology, Saarland University and Helmholtz Institute for Pharmaceutical Research Saarland (HIPS), Helmholtz Centre for Infection Research (HZI), 66123 Saarbrücken, Germany. rom@mx.uni-saarland.de.
Johannes HaybaeckInstitute of Pathology, Medical University of Graz, 8010 Graz, Austria. johannes.haybaeck@medunigraz.at.
Alexandra K KiemerDepartment of Pharmacy, Pharmaceutical Biology, Saarland University, Campus C2 2, 66123 Saarbrücken, Germany. pharm.bio.kiemer@mx.uni-saarland.de.
Saarland University · DEHelmholtz Centre for Infection Research · DELeibniz Research Centre for Working Environment and Human Factors · DEMedical University of Graz · ATTU Dortmund University · DEVrije Universiteit Amsterdam · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Non-alcoholic steatohepatitis (NASH) represents a risk factor for the development of hepatocellular carcinoma (HCC) and is characterized by quantitative and qualitative changes in hepatic lipids. Since elongation of fatty acids from C16 to C18 has recently been reported to promote both hepatic lipid accumulation and inflammation we aimed to investigate whether a frequently used mouse NASH model reflects this clinically relevant feature and whether C16 to C18 elongation can be observed in HCC development. Feeding mice a methionine and choline deficient diet to model NASH not only increased total hepatic fatty acids and cholesterol, but also distinctly elevated the C18/C16 ratio, which was not changed in a model of simple steatosis (ob/ob mice). Depletion of Kupffer cells abrogated both quantitative and qualitative methionine-and-choline deficient (MCD)-induced alterations in hepatic lipids. Interestingly, mimicking inflammatory events in early hepatocarcinogenesis by diethylnitrosamine-induced carcinogenesis (48 h) increased hepatic lipids and the C18/C16 ratio. Analyses of human liver samples from patients with NASH or NASH-related HCC showed an elevated expression of the elongase ELOVL6, which is responsible for the elongation of C16 fatty acids. Taken together, our findings suggest a detrimental role of an altered fatty acid pattern in the progression of NASH-related liver disease.

Indexed as

AcetyltransferasesAnimalsCarcinoma, HepatocellularCholineDietDiethylnitrosamineDisease Models, AnimalFatty Acid ElongasesFatty AcidsHumansInflammationLiver NeoplasmsMethionineMiceMice, Inbred DBAMice, ObeseAcetyltransferasesCholineDiethylnitrosamineELOVL6 protein, humanElovl6 protein, mouseFatty Acid ElongasesFatty AcidsMethionineRNA, Messenger

Identifiers

PMID24714086
PMCPMC4013594
OpenAlexW2049427440

What OpenQuestion holds

Textmetadata
LicenceCC BY
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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.