Evidence map›Paper›PMID 33006084›Full record

ReviewMolecular diagnosis & therapy2020

Genetic Determinants of Childhood Obesity.

Sheridan H Littleton, Robert I Berkowitz, Struan F A Grant

Open access · greenAbstract readReview
In one paragraph

Review in Molecular diagnosis & therapy, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed, 1 pooled it
7.9field-weighted citation impact, top 2% 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

52 citing papers in PubMed, 1 synthesis or guideline pooled it, 111 citations in OpenAlex.

  1. Pooled it
  2. Trial
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  5. Article
  6. Article
  7. Article
  8. Review
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  11. Article
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  14. Review
  15. Genetics of Common Obesity in Children and Adolescents.Annals of the New York Academy of Sciences · 2025
    Review
  16. Article
  17. Article
  18. Childhood obesity: The threatening apprentice of the adiposity empire.Reviews in endocrine & metabolic disorders · 2025
    Review
  19. Obesity and its management in primary care setting.Journal of diabetes and its complications · 2025
    Review
  20. Review
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

3 authors at 1 institution in 1 country.

Sheridan H LittletonCenter for Spatial and Functional Genomics, Children's Hospital of Philadelphia, Philadelphia, USA.
Robert I BerkowitzDepartment of Child and Adolescent Psychiatry and Behavioral Sciences, Children's Hospital of Philadelphia, Philadelphia, PA, 19104, USA.
Struan F A GrantCenter for Spatial and Functional Genomics, Children's Hospital of Philadelphia, Philadelphia, USA. grants@email.chop.edu.ORCID 0000-0003-2025-5302
Children's Hospital of Philadelphia · US

Funding

Genome Wide Association Study for Childhood ObesityR01HD056465 · NICHD · CHILDREN'S HOSP OF PHILADELPHIA · PI GRANT, STRUAN F A · 2008 to 2024
$9.5M
NICHD NIH HHS R01 HD056465
6 · The paper itself

Abstract

Obesity represents a major health burden to both developed and developing countries. Furthermore, the incidence of obesity is increasing in children. Obesity contributes substantially to mortality in the United States by increasing the risk for type 2 diabetes, cardiovascular-related diseases, and other comorbidities. Despite environmental changes over past decades, including increases in high-calorie foods and sedentary lifestyles, there is very clear evidence of a genetic predisposition to obesity risk. Childhood obesity cases can be categorized in one of two ways: syndromic or non-syndromic. Syndromic obesity includes disorders such as Prader-Willi syndrome, Bardet-Biedl syndrome, and Alström syndrome. Non-syndromic cases of obesity can be further separated into rarer instances of monogenic obesity and much more common forms of polygenic obesity. The advent of genome-wide association studies (GWAS) and next-generation sequencing has driven significant advances in our understanding of the genetic contribution to childhood obesity. Many rare and common genetic variants have been shown to contribute to the heritability in obesity, although the molecular mechanisms underlying most of these variants remain unclear. An important caveat of GWAS efforts is that they do not strictly represent gene target discoveries, rather simply the uncovering of robust genetic signals. One clear example of this is with progress in understanding the key obesity signal harbored within an intronic region of the FTO gene. It has been shown that the non-coding region in which the variant actually resides in fact influences the expression of genes distal to FTO instead, specifically IRX3 and IRX5. Such discoveries suggest that associated non-coding variants can be embedded within or next to one gene, but commonly influence the expression of other, more distal effector genes. Advances in genetics and genomics are therefore contributing to a deeper understanding of childhood obesity, allowing for development of clinical tools and therapeutic agents.

Indexed as

Genetic Predisposition to DiseaseChildGenetic VariationGenome-Wide Association StudyHumansMultifactorial InheritancePediatric ObesityRisk Factors

Identifiers

PMID33006084
PMCPMC7680380
OpenAlexW3091319413

What OpenQuestion holds

Textmetadata
LicenceTDM
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.