Evidence map›Paper›PMID 16021472›Full record

ArticleHuman genetics2005

Complex HTR2C linkage disequilibrium and promoter associations with body mass index and serum leptin.

Shane McCarthy, Salim Mottagui-Tabar, Yumi Mizuno, Bengt Sennblad, Johan Hoffstedt, Peter Arner, Claes Wahlestedt, Björn Andersson

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Article in Human genetics, 2005. 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
1.4field-weighted citation impact, top 22% 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, 36 citations in OpenAlex.

  1. Orexin, serotonin, and energy balance.WIREs mechanisms of disease · 2022
    Review
  2. Review
  3. Article
  4. The genetics of human obesity.Annals of the New York Academy of Sciences · 2013
    Review
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Medical sequencing at the extremes of human body mass.American journal of human genetics · 2007
    Article
  15. WEIGHT GAIN AND ANTIPSYCHOTICS. DATA FROM EUFEST STUDY.Acta endocrinologica (Bucharest, Romania : 2005)
    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

8 authors at 3 institutions in 1 country.

Shane McCarthyCenter for Genomics and Bioinformatics, Karolinska Institutet, Berzelius Väg 35, 17177 Stockholm, Sweden. shane.mccarthy@cgb.ki.se
Salim Mottagui-Tabar
Yumi Mizuno
Bengt Sennblad
Johan Hoffstedt
Peter Arner
Claes Wahlestedt
Björn Andersson
Karolinska Institutet · SEKarolinska University Hospital · SEAlbaNova · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The occurrence of obesity, eating disorders, and related diseases has increased in many parts of the world. Given that few strong genetic factors have been found, it is clear that these are complex multi-factorial diseases. The serotonin receptor 2C, a member of the 5-HTergic system, has been implicated in the control of phagia and obesity. We report a detailed investigation of linkage disequilibrium (LD) within and between the HTR2C promoter and the flanking sequences around a commonly utilized marker in the second coding exon of HTR2C. We suggest that inconsistent associations between HTR2C and several phenotypes, including obesity, may be due to the LD pattern across the gene in which recombination and gene conversion have been influential. The nucleotide and haplotype distribution is consistent with that of the neutral mutation model. The number of haplotypes suggests demographic influences or over dominant selection that may have a function in HTR2C expression. Using the fine LD pattern, we describe a possible association with promoter haplotypes and diplotypes, including a GT microsatellite, and body mass index (BMI) > or =30 kgm(-2) (P<0.0001). SNP -995G>A heterozygotes, as well as promoter diplotypes, were found to marginally influence higher serum leptin corrected for percentage body fat (P=0.01), which might suggest that these subjects are leptin resistant. Our results complement previous studies of HTR2C in both mice and humans, and suggest the importance of genetic variation and elucidating the fine LD structure in uncovering the genetic factors of obesity.

Indexed as

Body Mass IndexLinkage DisequilibriumPromoter Regions, GeneticAdultAgedHumansLeptinMaleMiddle AgedObesityPolymorphism, Single NucleotideReceptor, Serotonin, 5-HT2CReceptors, LeptinLEPR protein, humanLeptinReceptor, Serotonin, 5-HT2CReceptors, Leptin

Identifiers

PMID16021472
OpenAlexW2010925139

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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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.