Evidence map›Paper›PMID 26441656›Full record

ArticleFrontiers in pharmacology2015

Systems pharmacology of adiposity reveals inhibition of EP300 as a common therapeutic mechanism of caloric restriction and resveratrol for obesity.

Yuhei Nishimura, Shota Sasagawa, Michiko Ariyoshi, Sayuri Ichikawa, Yasuhito Shimada, Koki Kawaguchi, Reiko Kawase, Reiko Yamamoto, Takuma Uehara, Takaaki Yanai and 2 more

Open access · goldAbstract read
In one paragraph

Article in Frontiers in pharmacology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed, 1 pooled it
1.5field-weighted citation impact, top 18% 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

19 citing papers in PubMed, 1 synthesis or guideline pooled it, 34 citations in OpenAlex.

  1. Pooled it
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  11. The Potential to Fight Obesity with Adipogenesis Modulating Compounds.International journal of molecular sciences · 2022
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  14. Observational
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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

12 authors at 1 institution in 1 country.

Yuhei NishimuraDepartment of Molecular and Cellular Pharmacology, Pharmacogenomics and Pharmacoinformatics, Mie University Graduate School of Medicine Tsu, Japan ; Mie University Medical Zebrafish Research Center Tsu, Japan ; Department of Systems Pharmacology, Mie University Graduate School of Medicine Tsu, Japan ; Department of Omics Medicine, Mie University Industrial Technology Innovation Institute Tsu, Japan ; Department of Bioinformatics, Mie University Life Science Research Center Tsu, Japan.
Shota SasagawaDepartment of Molecular and Cellular Pharmacology, Pharmacogenomics and Pharmacoinformatics, Mie University Graduate School of Medicine Tsu, Japan.
Michiko AriyoshiDepartment of Molecular and Cellular Pharmacology, Pharmacogenomics and Pharmacoinformatics, Mie University Graduate School of Medicine Tsu, Japan.
Sayuri IchikawaDepartment of Molecular and Cellular Pharmacology, Pharmacogenomics and Pharmacoinformatics, Mie University Graduate School of Medicine Tsu, Japan.
Yasuhito ShimadaDepartment of Molecular and Cellular Pharmacology, Pharmacogenomics and Pharmacoinformatics, Mie University Graduate School of Medicine Tsu, Japan.
Koki KawaguchiDepartment of Molecular and Cellular Pharmacology, Pharmacogenomics and Pharmacoinformatics, Mie University Graduate School of Medicine Tsu, Japan.
Reiko KawaseDepartment of Molecular and Cellular Pharmacology, Pharmacogenomics and Pharmacoinformatics, Mie University Graduate School of Medicine Tsu, Japan.
Reiko YamamotoProduct Development Research Institute, Mercian Corporation Fujisawa, Japan.
Takuma UeharaProduct Development Research Institute, Mercian Corporation Fujisawa, Japan.
Takaaki YanaiProduct Development Research Institute, Mercian Corporation Fujisawa, Japan.
Ryoji TakataProduct Development Research Institute, Mercian Corporation Fujisawa, Japan.
Toshio TanakaDepartment of Molecular and Cellular Pharmacology, Pharmacogenomics and Pharmacoinformatics, Mie University Graduate School of Medicine Tsu, Japan ; Mie University Medical Zebrafish Research Center Tsu, Japan ; Department of Systems Pharmacology, Mie University Graduate School of Medicine Tsu, Japan ; Department of Omics Medicine, Mie University Industrial Technology Innovation Institute Tsu, Japan ; Department of Bioinformatics, Mie University Life Science Research Center Tsu, Japan.
Mie University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Both caloric restriction (CR) and resveratrol (RSV) have beneficial effects on obesity. However, the biochemical pathways that mediate these beneficial effects might be complex and interconnected and have not been fully elucidated. To reveal the common therapeutic mechanism of CR and RSV, we performed a comparative transcriptome analysis of adipose tissues from diet-induced obese (DIO) zebrafish and obese humans. We identified nine genes in DIO zebrafish and seven genes in obese humans whose expressions were regulated by CR and RSV. Although the gene lists did not overlap except for one gene, the gene ontologies enriched in the gene lists were highly overlapped, and included genes involved in adipocyte differentiation, lipid storage and lipid metabolism. Bioinformatic analysis of cis-regulatory sequences of these genes revealed that their transcriptional regulators also overlapped, including EP300, HDAC2, CEBPB, CEBPD, FOXA1, and FOXA2. We also identified 15 and 46 genes that were dysregulated in the adipose tissue of DIO zebrafish and obese humans, respectively. Bioinformatics analysis identified EP300, HDAC2, and CEBPB as common transcriptional regulators for these genes. EP300 is a histone and lysyl acetyltransferase that modulates the function of histone and various proteins including CEBPB, CEBPD, FOXA1, and FOXA2. We demonstrated that adiposity in larval zebrafish was significantly reduced by C646, an inhibitor of EP300 that antagonizes acetyl-CoA. The reduction of adiposity by C646 was not significantly different from that induced by RSV or co-treatment of C646 and RSV. These results indicate that the inhibition of EP300 might be a common therapeutic mechanism between CR and RSV in adipose tissues of obese individuals.

Indexed as

adipose tissuecaloric restrictioncomparative transcriptomeep300obesityresveratrolsystems pharmacologyzebrafish

Identifiers

PMID26441656
PMCPMC4569862
OpenAlexW1925501079

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.