Evidence map›Paper›PMID 31327168›Full record

ArticleMolecular nutrition & food research2019

Industrial Trans Fatty Acids Stimulate SREBP2-Mediated Cholesterogenesis and Promote Non-Alcoholic Fatty Liver Disease.

Antwi-Boasiako Oteng, Anke Loregger, Michel van Weeghel, Noam Zelcer, Sander Kersten

Open access · hybridAbstract read
In one paragraph

Article in Molecular nutrition & food research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
5.3field-weighted citation impact, top 4% 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

23 citing papers in PubMed, 43 citations in OpenAlex.

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  16. Omega-9 fatty acids: potential roles in inflammation and cancer management.Journal, genetic engineering & biotechnology · 2022
    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

5 authors at 3 institutions in 1 country.

Antwi-Boasiako OtengNutrition, Metabolism and Genomics Group, Division of Human Nutrition and Health, Wageningen University, 6708 WE, Wageningen, The Netherlands.ORCID 0000-0002-4879-065X
Anke LoreggerDepartment of Medical Biochemistry, Academic Medical Center, University of Amsterdam, 1105 AZ, Amsterdam, The Netherlands.
Michel van WeeghelLaboratory Genetic Metabolic Diseases, Amsterdam UMC, University of Amsterdam, Amsterdam Gastroenterology and Metabolism, Amsterdam Cardiovascular Sciences, 1105 AZ, Amsterdam, The Netherlands.
Noam ZelcerDepartment of Medical Biochemistry, Academic Medical Center, University of Amsterdam, 1105 AZ, Amsterdam, The Netherlands.
Sander KerstenNutrition, Metabolism and Genomics Group, Division of Human Nutrition and Health, Wageningen University, 6708 WE, Wageningen, The Netherlands.
Amsterdam UMC Location University of Amsterdam · NLWageningen University & Research · NLAmsterdam Neuroscience · NL

Funding

European Research Council 617376
6 · The paper itself

Abstract

scopeThe mechanisms underlying the deleterious effects of trans fatty acids on plasma cholesterol and non-alcoholic fatty liver disease (NAFLD) are unclear. Here, the aim is to investigate the molecular mechanisms of action of industrial trans fatty acids. METHODS AND

resultsHepa1-6 hepatoma cells were incubated with elaidate, oleate, or palmitate. C57Bl/6 mice were fed diets rich in trans-unsaturated, cis-unsaturated, or saturated fatty acids. Transcriptomics analysis of Hepa1-6 cells shows that elaidate but not oleate or palmitate induces expression of genes involved in cholesterol biosynthesis. Induction of cholesterogenesis by elaidate is mediated by increased sterol regulatory element-binding protein 2 (SREBP2) activity and is dependent on SREBP cleavage-activating protein (SCAP), yet independent of liver-X receptor and ubiquitin regulatory X domain-containing protein 8. Elaidate decreases intracellular free cholesterol levels and represses the anticholesterogenic effect of exogenous cholesterol. In mice, the trans-unsaturated diet increases the ratio of liver to gonadal fat mass, steatosis, hepatic cholesterol levels, alanine aminotransferase activity, and fibrosis markers, suggesting enhanced NAFLD, compared to the cis-unsaturated and saturated diets.

conclusionElaidate induces cholesterogenesis in vitro by activating the SCAP-SREBP2 axis, likely by lowering intracellular free cholesterol and attenuating cholesterol-dependent repression of SCAP. This pathway potentially underlies the increase in liver cholesterol and NAFLD by industrial trans fatty acids.

Indexed as

3T3-L1 CellsAnimalsCarcinoma, HepatocellularCell Line, TumorCHO CellsCholesterolCricetulusDietary FatsGene ExpressionIntracellular Signaling Peptides and ProteinsLiverMaleMembrane ProteinsMiceMice, Inbred C57BLNon-alcoholic Fatty Liver DiseaseCholesterolDietary Fatselaidic acidIntracellular Signaling Peptides and ProteinsMembrane ProteinsOleic AcidsSREBP cleavage-activating proteinSterol Regulatory Element Binding Protein 2Trans Fatty Acidscholesterogenesischolesterol metabolismelaidatenon-alcoholic fatty liver diseasesterol regulatory element binding proteins

Identifiers

PMID31327168
PMCPMC6790681
OpenAlexW2963413124

What Socratic 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 Socratic graph.