Evidence map›Paper›PMID 23762205›Full record

ReviewDeutsches Arzteblatt international2013

Molecular genetic aspects of weight regulation.

Johannes Hebebrand, Anke Hinney, Nadja Knoll, Anna-Lena Volckmar, André Scherag

Abstract readReview
In one paragraph

Review in Deutsches Arzteblatt international, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed, 1 pooled it
5.3field-weighted citation impact, top 4% 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

23 citing papers in PubMed, 1 synthesis or guideline pooled it, 84 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Article
  5. Observational
  6. Article
  7. Article
  8. Review
  9. Article
  10. [Twin research in Germany].Bundesgesundheitsblatt, Gesundheitsforschung, Gesundheitsschutz · 2021
    Review
  11. Review
  12. Article
  13. Review
  14. Article
  15. Article
  16. Review
  17. Review
  18. Review
  19. Gene-diet interaction and weight loss.Current opinion in lipidology · 2014
    Review
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

5 authors at 1 institution in 1 country.

Johannes HebebrandDepartment of Child and Adolescent Psychiatry, LVR-Klinikum Essen, University of Duisburg-Essen, Wickenburgstrasse 21, Essen, Germany. johannes.hebebrand@uni-due.de
Anke Hinney
Nadja Knoll
Anna-Lena Volckmar
André Scherag
University of Duisburg-Essen · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundFamily and twin studies have empirically revealed a 40% to 70% heritability of body-mass index, yet only a few hereditary factors have been identified to date that increase the risk of being overweight.

methodsWe present the current state of molecular genetic research on obesity with a selective review of the literature.

resultsA number of monogenic recessive mutations causing obesity have been identified, but these are rare. Various dominant mutations of the melanocortin-4 receptor gene are found in about 1% to 4% of all markedly obese persons. Current molecular genetic research focuses on the identification of common DNA variants affecting body weight; the genetic material of hundreds of thousands of people from around the world has now been investigated in genome-wide association studies. More than 30 variants conferring an increased risk have been identified, most of which are single nucleotide polymorphisms (SNPs) of no immediately clear functional significance. On average, these variants raise body weight by 500 g (range, 180 to 1400 g). Aside from SNPs, variations in the number of copies of specific DNA sequences have also been linked to obesity, as well as to subnormal weight. All the hereditary factors that have been identified to date account for about 5% of the variability of BMI. Extrapolation yields figures ranging from 10% to 15%.

conclusionsThe amount of genetic variability seen to date at the DNA level accounts only for a small fraction of the inter-individual variability of BMI. Obesity is thought to be a largely hereditary condition; the fact that its genetic basis has not yet been demonstrated may be due to various genetic or experimental factors.

Indexed as

Body WeightGenetic Predisposition to DiseaseHumansMutationObesityPolymorphism, Single NucleotidePrevalenceReceptor, Melanocortin, Type 4Risk AssessmentMC4R protein, humanReceptor, Melanocortin, Type 4

Identifiers

PMID23762205
PMCPMC3673040
OpenAlexW1480175372

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.