Evidence map›Paper›PMID 27288824›Full record

ReviewProgress in molecular biology and translational science2016

Single Gene and Syndromic Causes of Obesity: Illustrative Examples.

Merlin G Butler

Open access · greenAbstract readReview
In one paragraph

Review in Progress in molecular biology and translational science, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed, 1 pooled it
25.3field-weighted citation impact, top 1% 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

47 citing papers in PubMed, 1 synthesis or guideline pooled it, 70 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Trial
  4. Review
  5. Article
  6. Article
  7. Comprehending the Epidemiology and Aetiology of Childhood Obesity: Integrating Life Course Approaches for Prevention and Intervention.Diabetes therapy : research, treatment and education of diabetes and related disorders · 2025
    Review
  8. Review
  9. Review
  10. Treatment of Hypothalamic Obesity With GLP-1 Analogs.Journal of the Endocrine Society · 2024
    Review
  11. Review
  12. Review
  13. Article
  14. Review
  15. Article
  16. Autonomic nervous system dysfunction in Prader-Willi syndrome.Clinical autonomic research : official journal of the Clinical Autonomic Research Society · 2023
    Review
  17. Article
  18. Prader-Willi Syndrome and Chromosome 15q11.2 BP1-BP2 Region: A Review.International journal of molecular sciences · 2023
    Review
  19. Clinical Trials in Prader-Willi Syndrome: A Review.International journal of molecular sciences · 2023
    Review
  20. Chromosomal Microarray Study in Prader-Willi Syndrome.International journal of molecular sciences · 2023
    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

1 author at 1 institution in 1 country.

Merlin G ButlerDepartments of Psychiatry & Behavioral Sciences and Pediatrics, University of Kansas Medical Center, Kansas City, KS, United States of America. Electronic address: mbutler4@kumc.edu.
University of Kansas Medical Center · US

Funding

Research Design and Analysis Core (RDAC)P30HD002528 · NICHD · UNIVERSITY OF KANSAS LAWRENCE · PI FOWLER, STEPHEN CLETIUS · 1985 to 2015
$22.1M
NICHD NIH HHS P30 HD002528
6 · The paper itself

Abstract

Obesity is a significant health problem in westernized societies, particularly in the United States where it has reached epidemic proportions in both adults and children. The prevalence of childhood obesity has doubled in the past 30 years. The causation is complex with multiple sources, including an obesity promoting environment with plentiful highly dense food sources and overall decreased physical activity noted for much of the general population, but genetic factors clearly play a role. Advances in genetic technology using candidate gene approaches, genome-wide association studies, structural and expression microarrays, and next generation sequencing have led to the discovery of hundreds of genes recognized as contributing to obesity. Polygenic and monogenic causes of obesity are now recognized including dozens of examples of syndromic obesity with Prader-Willi syndrome, as a classical example and recognized as the most common known cause of life-threatening obesity. Genetic factors playing a role in the causation of obesity will be discussed along with the growing evidence of single genes and the continuum between monogenic and polygenic obesity. The clinical and genetic aspects of four classical but rare obesity-related syndromes (ie, Prader-Willi, Alström, fragile X, and Albright hereditary osteodystrophy) will be described and illustrated in this review of single gene and syndromic causes of obesity.

Indexed as

AdultGenetic Diseases, InbornGenetic Diseases, X-LinkedGenome-Wide Association StudyHigh-Throughput Nucleotide SequencingHumansObesityPrader-Willi SyndromeAlbright hereditary osteodystrophyAlström syndromecandidate obesity genesfragile X syndromegenomic imprintingPrader–Willi syndromesyndromic obesity

Identifiers

PMID27288824
PMCPMC7377403
OpenAlexW2339432153

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.