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Expression of epigenetic machinery genes is sensitive to maternal obesity and weight loss in relation to fetal growth in mice

Overview of attention for article published in Clinical Epigenetics, February 2016
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  • In the top 25% of all research outputs scored by Altmetric
  • High Attention Score compared to outputs of the same age (84th percentile)
  • High Attention Score compared to outputs of the same age and source (80th percentile)

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Title
Expression of epigenetic machinery genes is sensitive to maternal obesity and weight loss in relation to fetal growth in mice
Published in
Clinical Epigenetics, February 2016
DOI 10.1186/s13148-016-0188-3
Pubmed ID
Authors

Polina E. Panchenko, Sarah Voisin, Mélanie Jouin, Luc Jouneau, Audrey Prézelin, Simon Lecoutre, Christophe Breton, Hélène Jammes, Claudine Junien, Anne Gabory

Abstract

Maternal obesity impacts fetal growth and pregnancy outcomes. To counteract the deleterious effects of obesity on fertility and pregnancy issue, preconceptional weight loss is recommended to obese women. Whether this weight loss is beneficial/detrimental for offspring remains poorly explored. Epigenetic mechanisms could be affected by maternal weight changes, perturbing expression of key developmental genes in the placenta or fetus. Our aim was to investigate the effects of chronic maternal obesity on feto-placental growth along with the underlying epigenetic mechanisms. We also tested whether preconceptional weight loss could alleviate these effects. Female mice were fed either a control diet (CTRL group), a high-fat diet (obese (OB) group), or a high-fat diet switched to a control diet 2 months before conception (weight loss (WL) group). At mating, OB females presented an obese phenotype while WL females normalized metabolic parameters. At embryonic day 18.5 (E18.5), fetuses from OB females presented fetal growth restriction (FGR; -13 %) and 28 % of the fetuses were small for gestational age (SGA). Fetuses from WL females normalized this phenotype. The expression of 60 epigenetic machinery genes and 32 metabolic genes was measured in the fetal liver, placental labyrinth, and junctional zone. We revealed 23 genes altered by maternal weight trajectories in at least one of three tissues. The fetal liver and placental labyrinth were more responsive to maternal obesity than junctional zone. One third (18/60) of the epigenetic machinery genes were differentially expressed between at least two maternal groups. Interestingly, genes involved in the histone acetylation pathway were particularly altered (13/18). In OB group, lysine acetyltransferases and Bromodomain-containing protein 2 were upregulated, while most histone deacetylases were downregulated. In WL group, the expression of only a subset of these genes was normalized. This study highlights the high sensitivity of the epigenetic machinery gene expression, and particularly the histone acetylation pathway, to maternal obesity. These obesity-induced transcriptional changes could alter the placental and the hepatic epigenome, leading to FGR. Preconceptional weight loss appears beneficial to fetal growth, but some effects of previous obesity were retained in offspring phenotype.

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Mendeley readers

Mendeley readers

The data shown below were compiled from readership statistics for 120 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 120 100%

Demographic breakdown

Readers by professional status Count As %
Student > Ph. D. Student 30 25%
Student > Master 16 13%
Student > Bachelor 10 8%
Researcher 8 7%
Other 5 4%
Other 19 16%
Unknown 32 27%
Readers by discipline Count As %
Biochemistry, Genetics and Molecular Biology 25 21%
Agricultural and Biological Sciences 20 17%
Medicine and Dentistry 15 13%
Pharmacology, Toxicology and Pharmaceutical Science 7 6%
Neuroscience 3 3%
Other 13 11%
Unknown 37 31%
Attention Score in Context

Attention Score in Context

This research output has an Altmetric Attention Score of 12. This is our high-level measure of the quality and quantity of online attention that it has received. This Attention Score, as well as the ranking and number of research outputs shown below, was calculated when the research output was last mentioned on 17 March 2016.
All research outputs
#3,132,513
of 25,374,647 outputs
Outputs from Clinical Epigenetics
#216
of 1,436 outputs
Outputs of similar age
#47,107
of 311,886 outputs
Outputs of similar age from Clinical Epigenetics
#7
of 35 outputs
Altmetric has tracked 25,374,647 research outputs across all sources so far. Compared to these this one has done well and is in the 87th percentile: it's in the top 25% of all research outputs ever tracked by Altmetric.
So far Altmetric has tracked 1,436 research outputs from this source. They typically receive more attention than average, with a mean Attention Score of 8.4. This one has done well, scoring higher than 84% of its peers.
Older research outputs will score higher simply because they've had more time to accumulate mentions. To account for age we can compare this Altmetric Attention Score to the 311,886 tracked outputs that were published within six weeks on either side of this one in any source. This one has done well, scoring higher than 84% of its contemporaries.
We're also able to compare this research output to 35 others from the same source and published within six weeks on either side of this one. This one has done well, scoring higher than 80% of its contemporaries.