Evidence map›Paper›PMID 29434210›Full record

ArticleNature communications2018

Epigenetic modulation of Fgf21 in the perinatal mouse liver ameliorates diet-induced obesity in adulthood.

Xunmei Yuan, Kazutaka Tsujimoto, Koshi Hashimoto, Kenichi Kawahori, Nozomi Hanzawa, Miho Hamaguchi, Takami Seki, Makiko Nawa, Tatsuya Ehara, Yohei Kitamura and 8 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed
3.6field-weighted citation impact, top 6% 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

49 citing papers in PubMed, 82 citations in OpenAlex.

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  15. [Molecular pathological mechanism of liver metabolic disorder in mice with severe spinal muscular atrophy].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2023
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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

18 authors at 8 institutions in 1 country.

Xunmei YuanDepartment of Molecular Endocrinology and Metabolism, Tokyo Medical and Dental University, 1-5-45 Yushima, Bunkyo-ku, Tokyo, 113-8510, Japan.
Kazutaka TsujimotoDepartment of Molecular Endocrinology and Metabolism, Tokyo Medical and Dental University, 1-5-45 Yushima, Bunkyo-ku, Tokyo, 113-8510, Japan.
Koshi HashimotoDepartment of Preemptive Medicine and Metabolism, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University, 1-5-45 Yushima, Bunkyo-ku, Tokyo, 113-8510, Japan. khashimoto.mem@tmd.ac.jp.
Kenichi KawahoriDepartment of Molecular Endocrinology and Metabolism, Tokyo Medical and Dental University, 1-5-45 Yushima, Bunkyo-ku, Tokyo, 113-8510, Japan.
Nozomi HanzawaDepartment of Molecular Endocrinology and Metabolism, Tokyo Medical and Dental University, 1-5-45 Yushima, Bunkyo-ku, Tokyo, 113-8510, Japan.
Miho HamaguchiDepartment of Molecular Endocrinology and Metabolism, Tokyo Medical and Dental University, 1-5-45 Yushima, Bunkyo-ku, Tokyo, 113-8510, Japan.
Takami SekiDepartment of Molecular Endocrinology and Metabolism, Tokyo Medical and Dental University, 1-5-45 Yushima, Bunkyo-ku, Tokyo, 113-8510, Japan.
Makiko NawaLaboratory of Cytometry and Proteome Research, Nanken-Kyoten and Research Core Center, Tokyo Medical and Dental University, 1-5-45 Yushima, Bunkyo-ku, Tokyo, 113-8510, Japan.
Tatsuya EharaDepartment of Molecular Endocrinology and Metabolism, Tokyo Medical and Dental University, 1-5-45 Yushima, Bunkyo-ku, Tokyo, 113-8510, Japan.
Yohei KitamuraWellness and Nutrition Science Institute, Morinaga Milk Industry Co., Ltd, 5-1-83, Higashihara, Zama, Kanagawa, 252-8583, Japan.
Izuho HatadaLaboratory of Genome Science, Biosignal Genome Resource Center, Institute for Molecular and Cellular Regulation, Gunma University, 3-39-15 Showa-machi, Maebashi, Gunma, 371-8512, Japan.
Morichika KonishiDepartment of Microbial Chemistry, Kobe Pharmaceutical University, 1-19-4, Motoyama-kitamachi, Higashinada-ku, Kobe, Hyogo, 658-8558, Japan.
Nobuyuki ItohMedical Innovation Center, Kyoto University Graduate School of Medicine, 53 Kawahara-cho, Shogoin, Sakyo-ku, Kyoto, 606-8507, Japan.
Yoshimi NakagawaDepartment of Internal Medicine (Metabolism and Endocrinology), Faculty of Medicine, University of Tsukuba, 1-1-1 Tennodai, Tsukuba, Ibaraki, 305-8577, Japan.ORCID http://orcid.org/0000-0001-8710-5232
Hitoshi ShimanoDepartment of Internal Medicine (Metabolism and Endocrinology), Faculty of Medicine, University of Tsukuba, 1-1-1 Tennodai, Tsukuba, Ibaraki, 305-8577, Japan.
Takako Takai-IgarashiTohoku Medical Megabank Organization, 2-1 Seiryo-machi, Aoba-ku, Sendai, Miyagi, 980-8573, Japan.
Yasutomi KameiLaboratory of Molecular Nutrition, Graduate School of Life and Environmental Sciences, Kyoto Prefectural University, 1-5 Hangi-cho, Shimogamo, Sakyo-ku, Kyoto, 606-8522, Japan.
Yoshihiro OgawaDepartment of Molecular Endocrinology and Metabolism, Tokyo Medical and Dental University, 1-5-45 Yushima, Bunkyo-ku, Tokyo, 113-8510, Japan. yogawa@intmed3.med.kyushu-u.ac.jp.
Tokyo Medical and Dental University · JPUniversity of Tsukuba · JPGunma University · JPKobe Pharmaceutical University · JPKyoto Prefectural University · JPKyoto University · JPMorinaga (Japan) · JPTohoku Medical Megabank Organization · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The nutritional environment to which animals are exposed in early life can lead to epigenetic changes in the genome that influence the risk of obesity in later life. Here, we demonstrate that the fibroblast growth factor-21 gene (Fgf21) is subject to peroxisome proliferator-activated receptor (PPAR) α-dependent DNA demethylation in the liver during the postnatal period. Reductions in Fgf21 methylation can be enhanced via pharmacologic activation of PPARα during the suckling period. We also reveal that the DNA methylation status of Fgf21, once established in early life, is relatively stable and persists into adulthood. Reduced DNA methylation is associated with enhanced induction of hepatic FGF21 expression after PPARα activation, which may partly explain the attenuation of diet-induced obesity in adulthood. We propose that Fgf21 methylation represents a form of epigenetic memory that persists into adulthood, and it may have a role in the developmental programming of obesity.

Indexed as

Epigenesis, GeneticAnimalsDietDNA MethylationFemaleFibroblast Growth FactorsGene Expression RegulationHepatocytesHumansLiverMaleMiceObesityPPAR alphafibroblast growth factor 21Fibroblast Growth FactorsPPAR alpha

Identifiers

PMID29434210
PMCPMC5809372
OpenAlexW2795757307

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.