Evidence map›Paper›PMID 23664276›Full record

SynthesisAtherosclerosis2013

The shared allelic architecture of adiponectin levels and coronary artery disease.

Zari Dastani, Toby Johnson, Florian Kronenberg, Christopher P Nelson, Themistocles L Assimes, Winfried März, CARDIoGRAM Consortium, ADIPOGen Consortium, J Brent Richards

Abstract readMeta-Analysis
In one paragraph

Synthesis in Atherosclerosis, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
3.1field-weighted citation impact, top 8% 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

17 citing papers in PubMed, 37 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Effects of Adiponectin on T2DM and Glucose Homeostasis: A Mendelian Randomization Study.Diabetes, metabolic syndrome and obesity : targets and therapy · 2020
    Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Genetics of non-conventional lipoprotein fractions.Current genetic medicine reports · 2015
    Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Novel metabolic biomarkers of cardiovascular disease.Nature reviews. Endocrinology · 2014
    Review
  17. 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

9 authors at 7 institutions in 6 countries.

Zari DastaniDepartment of Epidemiology, Biostatistics and Occupational Health, Jewish General Hospital, Lady Davis Institute, McGill University Montreal, Quebec H3T 1E2, Canada.
Toby Johnson
Florian Kronenberg
Christopher P Nelson
Themistocles L Assimes
Winfried März
CARDIoGRAM Consortium
ADIPOGen Consortium
J Brent Richards
Innsbruck Medical University · ATJewish General Hospital · CAKing's College London · GBNational Institute for Health Research · GBSIB Swiss Institute of Bioinformatics · CHStanford University · USSynlab (Germany) · DE

Funding

COMMON VARIANTS IN CANDIDATE GENES AND PREMATURE MI RISKR01HL056931 · NHLBI · UNIVERSITY OF WASHINGTON · PI SCHWARTZ, STEPHEN MARC · 1998 to 2001
$1.5M
CIHRIntramural NIH HHS Z99 AG999999Wellcome Trust 090532Wellcome Trust 098498
6 · The paper itself

Abstract

objectiveA large body of epidemiologic data strongly suggests an association between excess adiposity and coronary artery disease (CAD). Low adiponectin levels, a hormone secreted only from adipocytes, have been associated with an increased risk of CAD in observational studies. However, these associations cannot clarify whether this relationship is causal or due to a shared set of causal factors or even confounding. Genome-wide association studies have identified common variants that influence adiponectin levels, providing valuable tools to examine the genetic relationship between adiponectin and CAD.

methodsUsing 145 genome wide significant SNPs for adiponectin from the ADIPOGen consortium (n = 49,891), we tested whether adiponectin-decreasing alleles influenced risk of CAD in the CARDIoGRAM consortium (n = 85,274).

resultsIn single-SNP analysis, 5 variants among 145 SNPs were associated with increased risk of CAD after correcting for multiple testing (P < 4.4 × 10(-4)). Using a multi-SNP genotypic risk score to test whether adiponectin levels and CAD have a shared genetic etiology, we found that adiponectin-decreasing alleles increased risk of CAD (P = 5.4 × 10(-7)).

conclusionThese findings demonstrate that adiponectin levels and CAD have a shared allelic architecture and provide rationale to undertake a Mendelian randomization studies to understand if this relationship is causal.

Indexed as

AdiponectinAdiposityAllelesAtherosclerosisCoronary Artery DiseaseDatabases, GeneticGenetic Predisposition to DiseaseGenome-Wide Association StudyGenotypeHumansMalePolymorphism, Single NucleotidePrevalenceRisk FactorsAdiponectinADIPOQ protein, human

Identifiers

PMID23664276
PMCPMC6139652
OpenAlexW2154649666

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.