You are seeing a free-to-access but limited selection of the activity Altmetric has collected about this research output.
Click here to find out more.
X Demographics
Mendeley readers
Attention Score in Context
| Title |
MEST mediates the impact of prenatal bisphenol A exposure on long-term body weight development
|
|---|---|
| Published in |
Clinical Epigenetics, April 2018
|
| DOI | 10.1186/s13148-018-0478-z |
| Pubmed ID | |
| Authors |
Kristin M. Junge, Beate Leppert, Susanne Jahreis, Dirk K. Wissenbach, Ralph Feltens, Konrad Grützmann, Loreen Thürmann, Tobias Bauer, Naveed Ishaque, Matthias Schick, Melanie Bewerunge-Hudler, Stefan Röder, Mario Bauer, Angela Schulz, Michael Borte, Kathrin Landgraf, Antje Körner, Wieland Kiess, Martin von Bergen, Gabriele I. Stangl, Saskia Trump, Roland Eils, Tobias Polte, Irina Lehmann |
| Abstract |
Exposure to endocrine-disrupting chemicals can alter normal physiology and increase susceptibility to non-communicable diseases like obesity. Especially the prenatal and early postnatal period is highly vulnerable to adverse effects by environmental exposure, promoting developmental reprogramming by epigenetic alterations. To obtain a deeper insight into the role of prenatal bisphenol A (BPA) exposure in children's overweight development, we combine epidemiological data with experimental models and BPA-dependent DNA methylation changes. BPA concentrations were measured in maternal urine samples of the LINA mother-child-study obtained during pregnancy (n = 552), and BPA-associated changes in cord blood DNA methylation were analyzed by Illumina Infinium HumanMethylation450 BeadChip arrays (n = 472). Methylation changes were verified by targeted MassARRAY analyses, assessed for their functional translation by qPCR and correlated with children's body mass index (BMI) z scores at the age of 1 and 6 years. Further, female BALB/c mice were exposed to BPA from 1 week before mating until delivery, and weight development of their pups was monitored (n ≥ 8/group). Additionally, human adipose-derived mesenchymal stem cells were treated with BPA during the adipocyte differentiation period and assessed for exposure-related epigenetic, transcriptional and morphological changes (n = 4). In prenatally BPA-exposed children two CpG sites with deviating cord blood DNA-methylation profiles were identified, among them a hypo-methylated CpG in the promoter of the obesity-associated mesoderm-specific transcript (MEST). A mediator analysis suggested that prenatal BPA exposure was connected to cord blood MEST promoter methylation and MEST expression as well as BMI z scores in early infancy. This effect could be confirmed in mice in which prenatal BPA exposure altered Mest promoter methylation and transcription with a concomitant increase in the body weight of the juvenile offspring. An experimental model of in vitro differentiated human mesenchymal stem cells also revealed an epigenetically induced MEST expression and enhanced adipogenesis following BPA exposure. Our study provides evidence that MEST mediates the impact of prenatal BPA exposure on long-term body weight development in offspring by triggering adipocyte differentiation. |
X Demographics
The data shown below were collected from the profiles of 2 X users who shared this research output. Click here to find out more about how the information was compiled.
Geographical breakdown
| Country | Count | As % |
|---|---|---|
| Spain | 2 | 100% |
Demographic breakdown
| Type | Count | As % |
|---|---|---|
| Members of the public | 2 | 100% |
Mendeley readers
The data shown below were compiled from readership statistics for 121 Mendeley readers of this research output. Click here to see the associated Mendeley record.
Geographical breakdown
| Country | Count | As % |
|---|---|---|
| Unknown | 121 | 100% |
Demographic breakdown
| Readers by professional status | Count | As % |
|---|---|---|
| Student > Ph. D. Student | 20 | 17% |
| Researcher | 16 | 13% |
| Student > Master | 16 | 13% |
| Student > Bachelor | 10 | 8% |
| Student > Postgraduate | 4 | 3% |
| Other | 13 | 11% |
| Unknown | 42 | 35% |
| Readers by discipline | Count | As % |
|---|---|---|
| Biochemistry, Genetics and Molecular Biology | 18 | 15% |
| Medicine and Dentistry | 17 | 14% |
| Nursing and Health Professions | 7 | 6% |
| Environmental Science | 6 | 5% |
| Social Sciences | 4 | 3% |
| Other | 17 | 14% |
| Unknown | 52 | 43% |
Attention Score in Context
This research output has an Altmetric Attention Score of 1. 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 01 May 2018.
All research outputs
#17,600,738
of 25,800,372 outputs
Outputs from Clinical Epigenetics
#1,011
of 1,454 outputs
Outputs of similar age
#221,335
of 341,687 outputs
Outputs of similar age from Clinical Epigenetics
#23
of 29 outputs
Altmetric has tracked 25,800,372 research outputs across all sources so far. This one is in the 21st percentile – i.e., 21% of other outputs scored the same or lower than it.
So far Altmetric has tracked 1,454 research outputs from this source. They typically receive more attention than average, with a mean Attention Score of 8.4. This one is in the 23rd percentile – i.e., 23% of its peers scored the same or lower than it.
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 341,687 tracked outputs that were published within six weeks on either side of this one in any source. This one is in the 26th percentile – i.e., 26% of its contemporaries scored the same or lower than it.
We're also able to compare this research output to 29 others from the same source and published within six weeks on either side of this one. This one is in the 17th percentile – i.e., 17% of its contemporaries scored the same or lower than it.