Evidence map›Paper›PMID 27034954›Full record

ArticleBioMed research international2016

Study of Valproic Acid-Enhanced Hepatocyte Steatosis.

Renin Chang, Mei-Chia Chou, Li-Ying Hung, Mu-En Wang, Meng-Chieh Hsu, Chih-Hsien Chiu

Open access · hybridAbstract read
In one paragraph

Article in BioMed research international, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.1field-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

13 citing papers in PubMed, 30 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

6 authors at 2 institutions in 1 country.

Renin ChangDepartment of Emergency Medicine, Kaohsiung Veterans General Hospital, No. 386, Dazhong 1st Road, Zuoying District, Kaohsiung 813, Taiwan.
Mei-Chia ChouDepartment of Physical Medicine and Rehabilitation, Kaohsiung Veterans General Hospital, Pingtung Branch, No. 1, Anpin 1st Lane, Jhaosheng Road, Longtan Village, Neipu Township, Pingtung County 912, Taiwan.
Li-Ying HungDepartment of Animal Science and Technology, National Taiwan University, No. 50, Lane 155, Sec. 3, Keelung Road, Taipei 106, Taiwan.
Mu-En WangDepartment of Animal Science and Technology, National Taiwan University, No. 50, Lane 155, Sec. 3, Keelung Road, Taipei 106, Taiwan.
Meng-Chieh HsuDepartment of Animal Science and Technology, National Taiwan University, No. 50, Lane 155, Sec. 3, Keelung Road, Taipei 106, Taiwan.
Chih-Hsien ChiuDepartment of Animal Science and Technology, National Taiwan University, No. 50, Lane 155, Sec. 3, Keelung Road, Taipei 106, Taiwan.
National Taiwan University of Science and Technology · TWKaohsiung Veterans General Hospital · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Valproic acid (VPA) is one of the most widely used antiepilepsy drugs. However, several side effects, including weight gain and fatty liver, have been reported in patients following VPA treatment. In this study, we explored the molecular mechanisms of VPA-induced hepatic steatosis using FL83B cell line-based in vitro model. Using fluorescent lipid staining technique, we found that VPA enhanced oleic acid- (OLA-) induced lipid accumulation in a dose-dependent manner in hepatocytes; this may be due to upregulated lipid uptake, triacylglycerol (TAG) synthesis, and lipid droplet formation. Real-time PCR results showed that, following VPA treatment, the expression levels of genes encoding cluster of differentiation 36 (Cd36), low-density lipoprotein receptor-related protein 1 (Lrp1), diacylglycerol acyltransferase 2 (Dgat2), and perilipin 2 (Plin2) were increased, that of carnitine palmitoyltransferase I a (Cpt1a) was not affected, and those of acetyl-Co A carboxylase α (Acca) and fatty acid synthase (Fasn) were decreased. Furthermore, using immunofluorescence staining and flow cytometry analyses, we found that VPA also induced peroxisome proliferator-activated receptor γ (PPARγ) nuclear translocation and increased levels of cell-surface CD36. Based on these results, we propose that VPA may enhance OLA-induced hepatocyte steatosis through the upregulation of PPARγ- and CD36-dependent lipid uptake, TAG synthesis, and lipid droplet formation.

Indexed as

CD36 AntigensDiacylglycerol O-AcyltransferaseFatty AcidsFatty LiverGene Expression RegulationHepatocytesHumansLipid MetabolismLipoproteins, LDLLow Density Lipoprotein Receptor-Related Protein-1Perilipin-2PPAR gammaTriglyceridesValproic AcidCD36 AntigensDGAT2 protein, humanDiacylglycerol O-AcyltransferaseFatty AcidsLipoproteins, LDLLow Density Lipoprotein Receptor-Related Protein-1LRP1 protein, humanPerilipin-2PLIN2 protein, humanPPAR gammaTriglyceridesValproic Acid

Identifiers

PMID27034954
PMCPMC4789392
OpenAlexW2285975527

What OpenQuestion holds

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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.