Evidence map›Paper›PMID 27252388›Full record

ArticleCirculation research2016

Role of Adiponectin in Coronary Heart Disease Risk: A Mendelian Randomization Study.

Maria Carolina Borges, Debbie A Lawlor, Cesar de Oliveira, Jon White, Bernardo Lessa Horta, Aluísio J D Barros

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Circulation research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
10.7field-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

42 citing papers in PubMed, 84 citations in OpenAlex.

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  7. The Plasma Levels of Protein Adiponectin (Diabetes, metabolic syndrome and obesity : targets and therapy · 2024
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  17. Adipocyte-Endothelium Crosstalk in Obesity.Frontiers in endocrinology · 2021
    Review
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 3 institutions in 2 countries.

Maria Carolina BorgesFrom the Postgraduate Program in Epidemiology, Federal University of Pelotas, Pelotas, Brazil (M.C.B., B.L.H., A.J.D.B.); MRC Integrative Epidemiology Unit (D.A.L.); School of Social and Community Medicine, University of Bristol, Bristol, United Kingdom (D.A.L.); and Epidemiology and Public Health, Institute of Epidemiology and Health Care (C.d.O.) and UCL Genetics Institute, Division of Biosciences, Faculty of Life Sciences (J.W.), University College London, London, United Kingdom. carolina.borges.mcb@gmail.com.
Debbie A LawlorFrom the Postgraduate Program in Epidemiology, Federal University of Pelotas, Pelotas, Brazil (M.C.B., B.L.H., A.J.D.B.); MRC Integrative Epidemiology Unit (D.A.L.); School of Social and Community Medicine, University of Bristol, Bristol, United Kingdom (D.A.L.); and Epidemiology and Public Health, Institute of Epidemiology and Health Care (C.d.O.) and UCL Genetics Institute, Division of Biosciences, Faculty of Life Sciences (J.W.), University College London, London, United Kingdom.
Cesar de OliveiraFrom the Postgraduate Program in Epidemiology, Federal University of Pelotas, Pelotas, Brazil (M.C.B., B.L.H., A.J.D.B.); MRC Integrative Epidemiology Unit (D.A.L.); School of Social and Community Medicine, University of Bristol, Bristol, United Kingdom (D.A.L.); and Epidemiology and Public Health, Institute of Epidemiology and Health Care (C.d.O.) and UCL Genetics Institute, Division of Biosciences, Faculty of Life Sciences (J.W.), University College London, London, United Kingdom.
Jon WhiteFrom the Postgraduate Program in Epidemiology, Federal University of Pelotas, Pelotas, Brazil (M.C.B., B.L.H., A.J.D.B.); MRC Integrative Epidemiology Unit (D.A.L.); School of Social and Community Medicine, University of Bristol, Bristol, United Kingdom (D.A.L.); and Epidemiology and Public Health, Institute of Epidemiology and Health Care (C.d.O.) and UCL Genetics Institute, Division of Biosciences, Faculty of Life Sciences (J.W.), University College London, London, United Kingdom.
Bernardo Lessa HortaFrom the Postgraduate Program in Epidemiology, Federal University of Pelotas, Pelotas, Brazil (M.C.B., B.L.H., A.J.D.B.); MRC Integrative Epidemiology Unit (D.A.L.); School of Social and Community Medicine, University of Bristol, Bristol, United Kingdom (D.A.L.); and Epidemiology and Public Health, Institute of Epidemiology and Health Care (C.d.O.) and UCL Genetics Institute, Division of Biosciences, Faculty of Life Sciences (J.W.), University College London, London, United Kingdom.
Aluísio J D BarrosFrom the Postgraduate Program in Epidemiology, Federal University of Pelotas, Pelotas, Brazil (M.C.B., B.L.H., A.J.D.B.); MRC Integrative Epidemiology Unit (D.A.L.); School of Social and Community Medicine, University of Bristol, Bristol, United Kingdom (D.A.L.); and Epidemiology and Public Health, Institute of Epidemiology and Health Care (C.d.O.) and UCL Genetics Institute, Division of Biosciences, Faculty of Life Sciences (J.W.), University College London, London, United Kingdom.
University of Bristol · GBMRC Epidemiology Unit · GBUniversidade Federal de Pelotas · BR

Funding

Project-001R01AG017644 · NIA · UNIVERSITY OF LONDON INST OF NEUROLOGY · PI Andrew Steptoe · 2000 to 2026
$56.2M
Medical Research Council MC_UU_12013/5NIA NIH HHS R01 AG017644
6 · The paper itself

Abstract

rationaleHypoadiponectinemia correlates with several coronary heart disease (CHD) risk factors. However, it is unknown whether adiponectin is causally implicated in CHD pathogenesis.

objectiveWe aimed to investigate the causal effect of adiponectin on CHD risk. METHODS AND

resultsWe undertook a Mendelian randomization study using data from genome-wide association studies consortia. We used the ADIPOGen consortium to identify genetic variants that could be used as instrumental variables for the effect of adiponectin. Data on the association of these genetic variants with CHD risk were obtained from CARDIoGRAM (22 233 CHD cases and 64 762 controls of European ancestry) and from CARDIoGRAMplusC4D Metabochip (63 746 cases and 130 681 controls; ≈ 91% of European ancestry) consortia. Data on the association of genetic variants with adiponectin levels and with CHD were combined to estimate the influence of blood adiponectin on CHD risk. In the conservative approach (restricted to using variants within the adiponectin gene as instrumental variables), each 1 U increase in log blood adiponectin concentration was associated with an odds ratio for CHD of 0.83 (95% confidence interval, 0.68-1.01) in CARDIoGRAM and 0.97 (95% confidence interval, 0.84-1.12) in CARDIoGRAMplusC4D Metabochip. Findings from the liberal approach (including variants in any locus across the genome) indicated a protective effect of adiponectin that was attenuated to the null after adjustment for known CHD predictors.

conclusionsOverall, our findings do not support a causal role of adiponectin levels in CHD pathogenesis.

Indexed as

AdiponectinCoronary DiseaseGenetic VariationGenome-Wide Association StudyHumansMendelian Randomization AnalysisPolymorphism, Single NucleotideRisk FactorsAdiponectinADIPOQ protein, humanadiponectincardiovascular diseasecoronary artery diseasemendelian randomization analysis obesity

Identifiers

PMID27252388
PMCPMC4959825
OpenAlexW2413926262

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.