Evidence map›Paper›PMID 23351195›Full record

ArticleBMC medical genetics2013

A comprehensive investigation of variants in genes encoding adiponectin (ADIPOQ) and its receptors (ADIPOR1/R2), and their association with serum adiponectin, type 2 diabetes, insulin resistance and the metabolic syndrome.

Kirsten E Peters, John Beilby, Gemma Cadby, Nicole M Warrington, David G Bruce, Wendy A Davis, Timothy Me Davis, Steven Wiltshire, Matthew Knuiman, Brendan M McQuillan and 3 more

Open access · goldAbstract read
In one paragraph

Article in BMC medical genetics, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed, 3 pooled it
7.7field-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

42 citing papers in PubMed, 3 syntheses or guidelines pooled it, 90 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Trial
  5. Review
  6. The Association Between Adiponectin Gene Polymorphism (rs1501299) and Metabolic Syndrome.Diabetes, metabolic syndrome and obesity : targets and therapy · 2025
    Article
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  9. Effect of Genetic Variations in theDiabetes, metabolic syndrome and obesity : targets and therapy · 2022
    Article
  10. Association ofDiabetes, metabolic syndrome and obesity : targets and therapy · 2022
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  18. Review
  19. [Association of +45 and +276 polymorphisms in the adiponectin gene with the development of Kawasaki disease].Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics · 2018
    Article
  20. 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

13 authors at 4 institutions in 2 countries.

Kirsten E PetersSchool of Medicine and Pharmacology, Fremantle Hospital Unit, The University of Western Australia, Nedlands, Western Australia, Australia.
John Beilby
Gemma Cadby
Nicole M Warrington
David G Bruce
Wendy A Davis
Timothy Me Davis
Steven Wiltshire
Matthew Knuiman
Brendan M McQuillan
Lyle J Palmer
Peter L Thompson
Joseph Hung
University of Western Australia · AUFremantle Hospital · AUOntario Institute for Cancer Research · CASir Charles Gairdner Hospital · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundLow levels of serum adiponectin have been linked to central obesity, insulin resistance, metabolic syndrome, and type 2 diabetes. Variants in ADIPOQ, the gene encoding adiponectin, have been shown to influence serum adiponectin concentration, and along with variants in the adiponectin receptors (ADIPOR1 and ADIPOR2) have been implicated in metabolic syndrome and type 2 diabetes. This study aimed to comprehensively investigate the association of common variants in ADIPOQ, ADIPOR1 and ADIPOR2 with serum adiponectin and insulin resistance syndromes in a large cohort of European-Australian individuals.

methodsSixty-four tagging single nucleotide polymorphisms in ADIPOQ, ADIPOR1 and ADIPOR2 were genotyped in two general population cohorts consisting of 2,355 subjects, and one cohort of 967 subjects with type 2 diabetes. The association of tagSNPs with outcomes were evaluated using linear or logistic modelling. Meta-analysis of the three cohorts was performed by random-effects modelling.

resultsMeta-analysis revealed nine genotyped tagSNPs in ADIPOQ significantly associated with serum adiponectin across all cohorts after adjustment for age, gender and BMI, including rs10937273, rs12637534, rs1648707, rs16861209, rs822395, rs17366568, rs3774261, rs6444175 and rs17373414. The results of haplotype-based analyses were also consistent. Overall, the variants in the ADIPOQ gene explained <5% of the variance in serum adiponectin concentration. None of the ADIPOR1/R2 tagSNPs were associated with serum adiponectin. There was no association between any of the genetic variants and insulin resistance or metabolic syndrome. A multi-SNP genotypic risk score for ADIPOQ alleles revealed an association with 3 independent SNPs, rs12637534, rs16861209, rs17366568 and type 2 diabetes after adjusting for adiponectin levels (OR=0.86, 95% CI=(0.75, 0.99), P=0.0134).

conclusionsGenetic variation in ADIPOQ, but not its receptors, was associated with altered serum adiponectin. However, genetic variation in ADIPOQ and its receptors does not appear to contribute to the risk of insulin resistance or metabolic syndrome but did for type 2 diabetes in a European-Australian population.

Indexed as

Polymorphism, Single NucleotideAdiponectinAdultAgedAustraliaDiabetes Mellitus, Type 2FemaleGenetic Association StudiesGenetic Predisposition to DiseaseHumansInsulin ResistanceMaleMetabolic SyndromeMiddle AgedReceptors, AdiponectinWhite PeopleAdiponectinReceptors, Adiponectin

Identifiers

PMID23351195
PMCPMC3598639
OpenAlexW2155723834

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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.