Evidence map›Paper›PMID 28543989›Full record

ArticleHuman brain mapping2017

Brain structural alterations in obese children with and without Prader-Willi Syndrome.

Mingze Xu, Yi Zhang, Karen M von Deneen, Huaiqiu Zhu, Jia-Hong Gao

Open access · bronzeAbstract read
In one paragraph

Article in Human brain mapping, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
2.0field-weighted citation impact, top 13% 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

15 citing papers in PubMed, 26 citations in OpenAlex.

  1. Article
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  7. Brain communications · 2022
    Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Review
  13. Review
  14. Obesity management in Prader-Willi syndrome: current perspectives.Diabetes, metabolic syndrome and obesity : targets and therapy · 2018
    Review
  15. Article
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

5 authors at 2 institutions in 2 countries.

Mingze XuCenter for MRI Research, Academy for Advanced Interdisciplinary Studies, Peking University, Beijing, 100871, China.
Yi ZhangCenter for Brain Imaging, Xidian University, Xi'an, 710071, China.
Karen M von DeneenCenter for Brain Imaging, Xidian University, Xi'an, 710071, China.
Huaiqiu ZhuDepartment of Biomedical Engineering, Peking University, Beijing, 100871, China.
Jia-Hong GaoCenter for MRI Research, Academy for Advanced Interdisciplinary Studies, Peking University, Beijing, 100871, China.ORCID 0000-0002-9311-0297
Peking University · CNXidian University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Prader-Willi syndrome (PWS) is a genetic imprinting disorder that is mainly characterized by hyperphagia and childhood obesity. Previous neuroimaging studies revealed that there is a significant difference in brain activation patterns between obese children with and without PWS. However, whether there are differences in the brain structure of obese children with and without PWS remains elusive. In the current study, we used T1-weighted and diffusion tensor magnetic resonance imaging to investigate alterations in the brain structure, such as the cortical volume and white matter integrity, in relation to this eating disorder in 12 children with PWS, 18 obese children without PWS (OB) and 18 healthy controls. Compared with the controls, both the PWS and OB groups exhibited alterations in cortical volume, with similar deficit patterns in 10 co-varying brain regions in the bilateral dorsolateral and medial prefrontal cortices, right anterior cingulate cortex, and bilateral temporal lobe. The white matter integrities of the above regions were then examined with an analysis method based on probabilistic tractography. The PWS group exhibited distinct changes in the reduced fractional anisotropy of white matter fibers connected to the co-varying regions, whereas the OB group did not. Our findings indicated that PWS and OB share similar gray matter alterations that are responsible for the development of eating disorders. Additionally, the distinct white matter alterations might explain the symptoms associated with food intake in PWS, including excessive hyperphagia and constant hunger. Hum Brain Mapp 38:4228-4238, 2017. © 2017 Wiley Periodicals, Inc.

Indexed as

Age FactorsBrainChildDiffusion Tensor ImagingFemaleGray MatterHumansMagnetic Resonance ImagingMaleNeural PathwaysObesityOrgan SizePrader-Willi SyndromeSex FactorsWhite Matterchildhood obesitycortical volumeeating disorderPrader-Willi syndrometractography

Identifiers

PMID28543989
PMCPMC6866858
OpenAlexW2617132639

What OpenQuestion holds

Textmetadata
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.