Evidence map›Paper›PMID 26052340›Full record

ArticleNutrition & metabolism2015

E2F8 promotes hepatic steatosis through FABP3 expression in diet-induced obesity in zebrafish.

Yasuhito Shimada, Shisei Kuninaga, Michiko Ariyoshi, Beibei Zhang, Yasuhiko Shiina, Yoshinori Takahashi, Noriko Umemoto, Yuhei Nishimura, Hiroyuki Enari, Toshio Tanaka

Open access · goldAbstract read
In one paragraph

Article in Nutrition & metabolism, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
2.0field-weighted citation impact, top 14% 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

24 citing papers in PubMed, 53 citations in OpenAlex.

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  7. Inhibition of polyploidization in Pten-deficient livers reduces steatosis.Liver international : official journal of the International Association for the Study of the Liver · 2022
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  17. The use of zebrafish (Animal frontiers : the review magazine of animal agriculture · 2019
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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

10 authors at 1 institution in 1 country.

Yasuhito ShimadaDepartment of Molecular and Cellular Pharmacology, Pharmacogenomics and Pharmacoinformatics, Mie University Graduate School of Medicine, 2-174, Edobashi, Tsu, Mie Japan ; Department of Systems Pharmacology, Mie University Graduate School of Medicine, Mie, Japan ; Mie University Medical Zebrafish Research Center, Mie, Japan ; Department of Bioinformatics, Mie University Life Science Research Center, Mie, Japan ; Department of Omics Medicine, Mie University Industrial Technology Innovation, Mie, Japan.
Shisei KuninagaCentral Research Institute, Maruha Nichiro Corporation, Ibaraki, Japan.
Michiko AriyoshiDepartment of Molecular and Cellular Pharmacology, Pharmacogenomics and Pharmacoinformatics, Mie University Graduate School of Medicine, 2-174, Edobashi, Tsu, Mie Japan.
Beibei ZhangDepartment of Molecular and Cellular Pharmacology, Pharmacogenomics and Pharmacoinformatics, Mie University Graduate School of Medicine, 2-174, Edobashi, Tsu, Mie Japan.
Yasuhiko ShiinaCentral Research Institute, Maruha Nichiro Corporation, Ibaraki, Japan.
Yoshinori TakahashiCentral Research Institute, Maruha Nichiro Corporation, Ibaraki, Japan.
Noriko UmemotoDepartment of Molecular and Cellular Pharmacology, Pharmacogenomics and Pharmacoinformatics, Mie University Graduate School of Medicine, 2-174, Edobashi, Tsu, Mie Japan ; Department of Systems Pharmacology, Mie University Graduate School of Medicine, Mie, Japan.
Yuhei NishimuraDepartment of Molecular and Cellular Pharmacology, Pharmacogenomics and Pharmacoinformatics, Mie University Graduate School of Medicine, 2-174, Edobashi, Tsu, Mie Japan ; Department of Systems Pharmacology, Mie University Graduate School of Medicine, Mie, Japan ; Mie University Medical Zebrafish Research Center, Mie, Japan ; Department of Bioinformatics, Mie University Life Science Research Center, Mie, Japan ; Department of Omics Medicine, Mie University Industrial Technology Innovation, Mie, Japan.
Hiroyuki EnariCentral Research Institute, Maruha Nichiro Corporation, Ibaraki, Japan.
Toshio TanakaDepartment of Molecular and Cellular Pharmacology, Pharmacogenomics and Pharmacoinformatics, Mie University Graduate School of Medicine, 2-174, Edobashi, Tsu, Mie Japan ; Department of Systems Pharmacology, Mie University Graduate School of Medicine, Mie, Japan ; Mie University Medical Zebrafish Research Center, Mie, Japan ; Department of Bioinformatics, Mie University Life Science Research Center, Mie, Japan ; Department of Omics Medicine, Mie University Industrial Technology Innovation, Mie, Japan.
Mie University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundDiet-induced hepatic steatosis is highly associated with nonalcoholic fatty liver disease, which is related to the development of metabolic syndrome. While advanced stage nonalcoholic hepatic steatosis and steatohepatitis (NASH) result ultimately in fibrosis and cirrhosis, the molecular basis for lipid droplet formation is poorly understood. Common pathways underlie the pathology of mammalian obesity and the zebrafish diet-induced obesity model (DIO-zebrafish) used in this study.

methodsOur analysis involved a combination of transcriptome (DNA microarray) and proteome (two-dimensional electrophoresis) methods using liver tissue from DIO-zebrafish to find candidate genes involved in hepatic steatosis. We conducted intraperitoneal injection (i.p.) of morpholino antisense oligonucleotides (MOs) for each gene into DIO-zebrafish. We also conducted in vitro overexpression in human cells. Additionally, we examined gene expression during feeding experiments involving anti-obesity compounds, creatine and anserine.

resultsWe found that fatty acid binding protein 3 (fabp3) and E2F transcription factors were upregulated in hepatic steatosis. E2f8 MO i.p. suppressed fabp3 expression in liver, and ameliorated hepatic steatosis. In human cells (HepG2), E2F8 overexpression promoted FABP3 expression. Additionally, co-administration of creatine and anserine suppressed obesity associated phenotypes including hepatic steatosis as indicated by e2f8 and fabp3 down regulation.

conclusionWe discovered that the e2f8-fabp3 axis is important in the promotion of hepatic steatosis in DIO-zebrafish. The combination of transcriptome and proteome analyses using the disease model zebrafish allow identification of novel pathways involved in human diseases.

Indexed as

Cross-species analysisDNA microarrayFatty liverHigh-fat feedingObesityTwo-dimensional electrophoresisZebrafish

Identifiers

PMID26052340
PMCPMC4456805
OpenAlexW1626664198

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Registered trials

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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.