Evidence map›Paper›PMID 26868178›Full record

ArticleScientific reports2016

Gene expression profiling of white adipose tissue reveals paternal transmission of proneness to obesity.

Sumiyo Morita, Kazuhiko Nakabayashi, Tomoko Kawai, Keiko Hayashi, Takuro Horii, Mika Kimura, Yasutomi Kamei, Yoshihiro Ogawa, Kenichiro Hata, Izuho Hatada

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
2.1field-weighted citation impact, top 12% 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

6 citing papers in PubMed, 8 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

10 authors at 4 institutions in 1 country.

Sumiyo MoritaLaboratory of Genome Science, Biosignal Genome Resource Center, Institute for Molecular and Cellular Regulation, Gunma University, 3-39-15 Showa-machi Maebashi, 371-8512, Japan.
Kazuhiko NakabayashiDepartment of Maternal-Fetal Biology, National Research Institute for Child Health and Development, 2-10-1 Okura Setagaya-ku Tokyo, 157-8535, Japan.
Tomoko KawaiDepartment of Maternal-Fetal Biology, National Research Institute for Child Health and Development, 2-10-1 Okura Setagaya-ku Tokyo, 157-8535, Japan.
Keiko HayashiDepartment of Maternal-Fetal Biology, National Research Institute for Child Health and Development, 2-10-1 Okura Setagaya-ku Tokyo, 157-8535, Japan.
Takuro HoriiLaboratory of Genome Science, Biosignal Genome Resource Center, Institute for Molecular and Cellular Regulation, Gunma University, 3-39-15 Showa-machi Maebashi, 371-8512, Japan.
Mika KimuraLaboratory of Genome Science, Biosignal Genome Resource Center, Institute for Molecular and Cellular Regulation, Gunma University, 3-39-15 Showa-machi Maebashi, 371-8512, Japan.
Yasutomi KameiLaboratory of Molecular Nutrition, Graduate School of Environmental and Life Science, Kyoto Prefectural University, 1-5 Hangi-cho, Shimogamo, Sakyo-ku, Kyoto, 606-8522, Japan.
Yoshihiro OgawaDepartment of Molecular Endocrinology and Metabolism, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University, 1-5-45 Bunkyo-ku, Yushima, Tokyo, 113-8510, Japan.
Kenichiro HataDepartment of Maternal-Fetal Biology, National Research Institute for Child Health and Development, 2-10-1 Okura Setagaya-ku Tokyo, 157-8535, Japan.
Izuho HatadaLaboratory of Genome Science, Biosignal Genome Resource Center, Institute for Molecular and Cellular Regulation, Gunma University, 3-39-15 Showa-machi Maebashi, 371-8512, Japan.
Gunma University · JPNational Center For Child Health and Development · JPKyoto Prefectural University · JPTokyo Medical and Dental University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Previously, we found that C57BL/6J (B6) mice are more prone to develop obesity than PWK mice. In addition, we analyzed reciprocal crosses between these mice and found that (PWK × B6) F1 mice, which have B6 fathers, are more likely to develop dietary obesity than (B6 × PWK) F1 mice, which have B6 mothers. These results suggested that diet-induced obesity is paternally transmitted. In this study, we performed transcriptome analysis of adipose tissues of B6, PWK, (PWK × B6) F1, and (B6 × PWK) F1 mice using next-generation sequencing. We found that paternal transmission of diet-induced obesity was correlated with genes involved in adipose tissue inflammation, metal ion transport, and cilia. Furthermore, we analyzed the imprinted genes expressed in white adipose tissue (WAT) and obesity. Expression of paternally expressed imprinted genes (PEGs) was negatively correlated with body weight, whereas expression of maternally expressed imprinted genes (MEGs) was positively correlated. In the obesity-prone B6 mice, expression of PEGs was down-regulated by a high-fat diet, suggesting that abnormally low expression of PEGs contributes to high-fat diet-induced obesity in B6 mice. In addition, using single-nucleotide polymorphisms that differ between B6 and PWK, we identified candidate imprinted genes in WAT.

Indexed as

Gene Expression ProfilingPaternal InheritanceAdipose Tissue, WhiteAnimalsDietHigh-Throughput Nucleotide SequencingMaleMice, Inbred C57BLObesityPolymorphism, Single Nucleotide

Identifiers

PMID26868178
PMCPMC4751506
OpenAlexW2410598136

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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.