Evidence map›Paper›PMID 22399527›Full record

SynthesisCirculation. Cardiovascular genetics2012

Genome-wide screen for metabolic syndrome susceptibility Loci reveals strong lipid gene contribution but no evidence for common genetic basis for clustering of metabolic syndrome traits.

Kati Kristiansson, Markus Perola, Emmi Tikkanen, Johannes Kettunen, Ida Surakka, Aki S Havulinna, Alena Stancáková, Chris Barnes, Elisabeth Widen, Eero Kajantie and 24 more

Open access · bronzeAbstract readMeta-Analysis
In one paragraph

Synthesis in Circulation. Cardiovascular genetics, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 115 papers, 13 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
115citing papers in PubMed, 13 pooled it
15.3field-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

115 citing papers in PubMed, 13 syntheses or guidelines pooled it, 209 citations in OpenAlex.

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  9. Pleiotropic genes for metabolic syndrome and inflammation.Molecular genetics and metabolism · 2014
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  19. Central Obesity is Associated with Increased Left Ventricular Maximal Wall Thickness and Intrathoracic Adipose Tissue Measured with Cardiac Magnetic Resonance.High blood pressure & cardiovascular prevention : the official journal of the Italian Society of Hypertension · 2024
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55 more citing papers are in PubMed but not listed here.

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

34 authors at 6 institutions in 5 countries.

Kati KristianssonNational Institute for Health and Welfare, University of Helsinki, Biomedicum, Helsinki, Finland. kati.kristiansson@thl.fi
Markus Perola
Emmi Tikkanen
Johannes Kettunen
Ida Surakka
Aki S Havulinna
Alena Stancáková
Chris Barnes
Elisabeth Widen
Eero Kajantie
Johan G Eriksson
Jorma Viikari
Mika Kähönen
Terho Lehtimäki
Olli T Raitakari
Anna-Liisa Hartikainen
Aimo Ruokonen
Anneli Pouta
Antti Jula
Antti J Kangas
Pasi Soininen
Mika Ala-Korpela
Satu Männistö
Pekka Jousilahti
Lori L Bonnycastle
Marjo-Riitta Järvelin
Johanna Kuusisto
Francis S Collins
Markku Laakso
Matthew E Hurles
Aarno Palotie
Leena Peltonen
Samuli Ripatti
Veikko Salomaa
Agaplesion Markus Hospital · DEBarnes Hospital · GBElisa (Finland) · FIFinnish Institute for Health and Welfare · FIKrankenhaus der Elisabethinen · ATS:t Eriks Ögonsjukhus · SE

Funding

Genetic analysis of type II diabetes in Finnish populationZIAHG000024 · NHGRI · NATIONAL HUMAN GENOME RESEARCH INSTITUTE · PI ERDOS, MICHAEL · 2009 to 2025
$38.2M
Wellcome Trust 069224
6 · The paper itself

Abstract

backgroundGenome-wide association (GWA) studies have identified several susceptibility loci for metabolic syndrome (MetS) component traits, but have had variable success in identifying susceptibility loci to the syndrome as an entity. We conducted a GWA study on MetS and its component traits in 4 Finnish cohorts consisting of 2637 MetS cases and 7927 controls, both free of diabetes, and followed the top loci in an independent sample with transcriptome and nuclear magnetic resonance-based metabonomics data. Furthermore, we tested for loci associated with multiple MetS component traits using factor analysis, and built a genetic risk score for MetS. METHODS AND

resultsA previously known lipid locus, APOA1/C3/A4/A5 gene cluster region (SNP rs964184), was associated with MetS in all 4 study samples (P=7.23×10(-9) in meta-analysis). The association was further supported by serum metabolite analysis, where rs964184 was associated with various very low density lipoprotein, triglyceride, and high-density lipoprotein metabolites (P=0.024-1.88×10(-5)). Twenty-two previously identified susceptibility loci for individual MetS component traits were replicated in our GWA and factor analysis. Most of these were associated with lipid phenotypes, and none with 2 or more uncorrelated MetS components. A genetic risk score, calculated as the number of risk alleles in loci associated with individual MetS traits, was strongly associated with MetS status.

conclusionsOur findings suggest that genes from lipid metabolism pathways have the key role in the genetic background of MetS. We found little evidence for pleiotropy linking dyslipidemia and obesity to the other MetS component traits, such as hypertension and glucose intolerance.

Indexed as

Genetic Predisposition to DiseaseGenome-Wide Association StudyLipid MetabolismAdultFemaleHumansMaleMetabolic SyndromeMiddle AgedPolymorphism, Single NucleotideRisk Factors

Identifiers

PMID22399527
PMCPMC3378651
OpenAlexW2098238559

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.