Evidence map›Paper›PMID 27167736›Full record

ArticlePloS one2016

Susceptibility of Different Mouse Wild Type Strains to Develop Diet-Induced NAFLD/AFLD-Associated Liver Disease.

Vera H I Fengler, Tanja Macheiner, Sonja M Kessler, Beate Czepukojc, Katja Gemperlein, Rolf Müller, Alexandra K Kiemer, Christoph Magnes, Johannes Haybaeck, Carolin Lackner and 1 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.

0numbers the graph read from it
0cells of the map it votes in
56citing papers in PubMed
6.7field-weighted citation impact, top 3% 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

56 citing papers in PubMed, 73 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

11 authors at 4 institutions in 2 countries.

Vera H I FenglerBioPersMed/Biobank Graz, Medical University of Graz, Graz, Austria.
Tanja MacheinerBioPersMed/Biobank Graz, Medical University of Graz, Graz, Austria.
Sonja M KesslerDepartment of Pharmacy, Pharmaceutical Biology, Saarland University, Saarbrücken, Germany.
Beate CzepukojcDepartment of Pharmacy, Pharmaceutical Biology, Saarland University, Saarbrücken, Germany.
Katja GemperleinDepartment of Pharmacy, Pharmaceutical Biotechnology, Saarland University, Saarbrücken, Germany.
Rolf MüllerDepartment of Pharmacy, Pharmaceutical Biotechnology, Saarland University, Saarbrücken, Germany.
Alexandra K KiemerDepartment of Pharmacy, Pharmaceutical Biology, Saarland University, Saarbrücken, Germany.
Christoph MagnesInstitute for Biomedicine and Health Sciences, Joanneum Research, Graz, Austria.
Johannes HaybaeckInstitute of Pathology, Medical University of Graz, Graz, Austria.
Carolin LacknerInstitute of Pathology, Medical University of Graz, Graz, Austria.
Karine SargsyanBioPersMed/Biobank Graz, Medical University of Graz, Graz, Austria.
Medical University of Graz · ATSaarland University · DEHelmholtz Centre for Infection Research · DEJoanneum Research · AT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Although non-alcoholic and alcoholic fatty liver disease have been intensively studied, concerning pathophysiological mechanisms are still incompletely understood. This may be due to the use of different animal models and resulting model-associated variation. Therefore, this study aimed to compare three frequently used wild type mouse strains in their susceptibility to develop diet-induced features of non-alcoholic/alcoholic fatty liver disease. Fatty liver disease associated clinical, biochemical, and histological features in C57BL/6, CD-1, and 129Sv WT mice were induced by (i) high-fat diet feeding, (ii) ethanol feeding only, and (iii) the combination of high-fat diet and ethanol feeding. Hepatic and subcutaneous adipose lipid profiles were compared in CD-1 and 129Sv mice. Additionally hepatic fatty acid composition was determined in 129Sv mice. In C57BL/6 mice dietary regimens resulted in heterogeneous hepatic responses, ranging from pronounced steatosis and inflammation to a lack of any features of fatty liver disease. Liver-related serum biochemistry showed high deviations within the regimen groups. CD-1 mice did not exhibit significant changes in metabolic and liver markers and developed no significant steatosis or inflammation as a response to dietary regimens. Although 129Sv mice showed no weight gain, this strain achieved most consistent features of fatty liver disease, apparent from concentration alterations of liver-related serum biochemistry as well as moderate steatosis and inflammation as a result of all dietary regimens. Furthermore, the hepatic lipid profile as well as the fatty acid composition of 129Sv mice were considerably altered, upon feeding the different dietary regimens. Accordingly, diet-induced non-alcoholic/alcoholic fatty liver disease is most consistently promoted in 129Sv mice compared to C57BL/6 and CD-1 mice. As a conclusion, this study demonstrates the importance of genetic background of used mouse strains for modeling diet-induced non-alcoholic/alcoholic fatty liver disease.

Indexed as

Disease SusceptibilityAlanine TransaminaseAnimalsAspartate AminotransferasesBiomarkersCholesterolDietary FatsDiet, High-FatDisease Models, AnimalEthanolFatty Acids, NonesterifiedFatty Liver, AlcoholicLiverLiver Function TestsMaleMiceAlanine TransaminaseAspartate AminotransferasesBiomarkersCholesterolDietary FatsEthanolFatty Acids, NonesterifiedTriglycerides

Identifiers

PMID27167736
PMCPMC4863973
OpenAlexW2366997102

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.