Evidence map›Paper›PMID 21771975›Full record

ArticleDiabetes2011

A genome-wide association study reveals a quantitative trait locus of adiponectin on CDH13 that predicts cardiometabolic outcomes.

Chia-Min Chung, Tsung-Hsien Lin, Jaw-Wen Chen, Hsin-Bang Leu, Hsin-Chou Yang, Hung-Yun Ho, Chih-Tai Ting, Sheng-Hsiung Sheu, Wei-Chuan Tsai, Jyh-Hong Chen and 3 more

Open access · bronzeAbstract read
In one paragraph

Article in Diabetes, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 74 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
74citing papers in PubMed, 3 pooled it
7.2field-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

74 citing papers in PubMed, 3 syntheses or guidelines pooled it, 127 citations in OpenAlex.

  1. Pooled it
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  7. T-cadherin, a major adiponectin binding partner, suppresses ERK signaling in metabolic tissues.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
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  11. Cancer biology & therapy · 2024
    Article
  12. [Genotype-environment interaction on arterial stiffness: A pedigree-based study].Beijing da xue xue bao. Yi xue ban = Journal of Peking University. Health sciences · 2023
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14 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

13 authors at 8 institutions in 1 country.

Chia-Min ChungInstitute of Biomedical Sciences, Academia Sinica, Taipei, Taiwan.
Tsung-Hsien Lin
Jaw-Wen Chen
Hsin-Bang Leu
Hsin-Chou Yang
Hung-Yun Ho
Chih-Tai Ting
Sheng-Hsiung Sheu
Wei-Chuan Tsai
Jyh-Hong Chen
Shing-Jong Lin
Yuan-Tsong Chen
Wen-Harn Pan
Institute of Biomedical Sciences, Academia Sinica · TWNational Cheng Kung University · TWTaichung Veterans General Hospital · TWTaipei Veterans General Hospital · TWInstitute of Statistical Science, Academia Sinica · TWKaohsiung Medical University · TWKaohsiung Medical University Chung-Ho Memorial Hospital · TWNational Yang Ming Chiao Tung University · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveThe plasma adiponectin level, a potential upstream and internal facet of metabolic and cardiovascular diseases, has a reasonably high heritability. Whether other novel genes influence the variation in adiponectin level and the roles of these genetic variants on subsequent clinical outcomes has not been thoroughly investigated. Therefore, we aimed not only to identify genetic variants modulating plasma adiponectin levels but also to investigate whether these variants are associated with adiponectin-related metabolic traits and cardiovascular diseases. RESEARCH DESIGN AND

methodsWe conducted a genome-wide association study (GWAS) to identify quantitative trait loci (QTL) associated with high molecular weight forms of adiponectin levels by genotyping 382 young-onset hypertensive (YOH) subjects with Illumina HumanHap550 SNP chips. The culpable single nucleotide polymorphism (SNP) variants responsible for lowered adiponectin were then confirmed in another 559 YOH subjects, and the association of these SNP variants with the risk of metabolic syndrome (MS), type 2 diabetes mellitus (T2DM), and ischemic stroke was examined in an independent community-based prospective cohort, the CardioVascular Disease risk FACtors Two-township Study (CVDFACTS, n = 3,350).

resultsThe SNP (rs4783244) most significantly associated with adiponectin levels was located in intron 1 of the T-cadherin (CDH13) gene in the first stage (P = 7.57 × 10(-9)). We replicated and confirmed the association between rs4783244 and plasma adiponectin levels in an additional 559 YOH subjects (P = 5.70 × 10(-17)). This SNP was further associated with the risk of MS (odds ratio [OR] = 1.42, P = 0.027), T2DM in men (OR = 3.25, P = 0.026), and ischemic stroke (OR = 2.13, P = 0.002) in the CVDFACTS.

conclusionsThese findings indicated the role of T-cadherin in modulating adiponectin levels and the involvement of CDH13 or adiponectin in the development of cardiometabolic diseases.

Indexed as

Genetic Predisposition to DiseaseQuantitative Trait LociAdiponectinAdultBlood GlucoseBrain IschemiaCadherinsDiabetes Mellitus, Type 2FemaleGenome-Wide Association StudyGenotypeHumansHypertensionMaleMetabolic SyndromePolymorphism, Single NucleotideAdiponectinBlood GlucoseCadherinsH-cadherin

Identifiers

PMID21771975
PMCPMC3161336
OpenAlexW2103979085

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.