Evidence map›Paper›PMID 42032377›Full record

ArticleDiabetologia2026

Causal relationship between epigenetic markers and type 2 diabetes in West African populations: a Mendelian randomisation analysis.

Karlijn A C Meeks, Eva L van der Linden, Amy R Bentley, Ayo P Doumatey, Peter Henneman, Nora Franceschini, Themistocles L Assimes, Felix P Chilunga, Charles F Hayfron-Benjamin, Ellis Owusu-Dabo and 4 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Diabetologia, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

14 authors.

Karlijn A C MeeksCenter for Research on Genomics and Global Health, National Human Genome Research Institute, National Institutes of Health, Bethesda, MD, USA. karlijn.meeks@som.umaryland.edu.ORCID http://orcid.org/0000-0003-3032-405X
Eva L van der LindenDepartment of Public and Occupational Health, Amsterdam UMC, University of Amsterdam, Amsterdam Public Health Research Institute, Amsterdam, the Netherlands.ORCID http://orcid.org/0000-0002-4037-1717
Amy R BentleyCenter for Research on Genomics and Global Health, National Human Genome Research Institute, National Institutes of Health, Bethesda, MD, USA.ORCID http://orcid.org/0000-0002-0827-9101
Ayo P DoumateyCenter for Research on Genomics and Global Health, National Human Genome Research Institute, National Institutes of Health, Bethesda, MD, USA.ORCID http://orcid.org/0000-0001-9494-7710
Peter HennemanDepartment of Human Genetics, Epigenetics, Reproduction & Development, Amsterdam UMC, University of Amsterdam, Amsterdam, the Netherlands.ORCID http://orcid.org/0000-0003-2179-7808
Nora FranceschiniDepartment of Epidemiology, University of North Carolina, Chapel Hill, NC, USA.ORCID http://orcid.org/0009-0001-8346-3662
Themistocles L AssimesDepartment of Medicine, Stanford University School of Medicine, Stanford, CA, USA.ORCID http://orcid.org/0000-0003-2349-0009
Felix P ChilungaDepartment of Public and Occupational Health, Amsterdam UMC, University of Amsterdam, Amsterdam Public Health Research Institute, Amsterdam, the Netherlands.ORCID http://orcid.org/0000-0003-4083-001X
Charles F Hayfron-BenjaminDepartment of Public and Occupational Health, Amsterdam UMC, University of Amsterdam, Amsterdam Public Health Research Institute, Amsterdam, the Netherlands.ORCID http://orcid.org/0000-0003-0175-0340
Ellis Owusu-DaboDepartment of Global and International Health, School of Public Health, Kwame Nkrumah University of Science and Technology, Kumasi, Ghana.ORCID http://orcid.org/0000-0003-4232-4292
Guanjie ChenCenter for Research on Genomics and Global Health, National Human Genome Research Institute, National Institutes of Health, Bethesda, MD, USA.ORCID http://orcid.org/0000-0002-5745-5618
Charles AgyemangDepartment of Public and Occupational Health, Amsterdam UMC, University of Amsterdam, Amsterdam Public Health Research Institute, Amsterdam, the Netherlands.ORCID http://orcid.org/0000-0002-3882-7295
Adebowale A AdeyemoCenter for Research on Genomics and Global Health, National Human Genome Research Institute, National Institutes of Health, Bethesda, MD, USA.ORCID http://orcid.org/0000-0002-3105-3231
Charles N RotimiCenter for Research on Genomics and Global Health, National Human Genome Research Institute, National Institutes of Health, Bethesda, MD, USA. rotimic@mail.nih.gov.ORCID http://orcid.org/0000-0001-5759-053X

Funding

Genetic epidemiology of complex diseasesZ01HG200362 · NHGRI · NATIONAL HUMAN GENOME RESEARCH INSTITUTE · PI ROTIMI, CHARLES · 2008 to 2008
$1.7M
Division of Diabetes, Endocrinology, and Metabolic Diseases DK131018NIH Office of the Director Z01HG200362Office of Research on Minority Health 3T37TW00041-03S2Seventh Framework Programme 278901
6 · The paper itself

Abstract

aims/hypothesisEvidence for a causal role of DNA methylation sites (CpGs) in type 2 diabetes and glycaemic traits is limited due to the cross-sectional nature of many epigenome-wide association studies (EWAS). In addition, epigenetic studies in West African populations are particularly sparse, despite the high and rising burden of type 2 diabetes in these populations. Hence, we aimed to identify CpGs causally associated with type 2 diabetes among West Africans by leveraging Mendelian randomisation (MR) analysis and longitudinal data.

methodsWe used the Illumina EPIC DNA methylation array to profile the methylation of DNA extracted from white blood cells collected from 879 Ghanaian individuals (the Research on Obesity and Diabetes among African Migrants [RODAM] study) and 332 Nigerian individuals (the Africa America Diabetes Mellitus [AADM] study) who were not on glucose-lowering medication. We carried forwards CpGs identified in EWAS for type 2 diabetes and meta-analysed EWAS for HbA

resultsWe identified 28 CpGs associated with type 2 diabetes, 26 with HbA CONCLUSIONS/

interpretationOur study identified two epigenetic markers as likely to be causal for type 2 diabetes in West African populations. In addition to enhancing our understanding of disease mechanisms, these CpGs with evidence of causal associations could be prioritised as potential biomarkers for early detection of disease or as drug development targets.

Indexed as

Diabetes Mellitus, Type 2Epigenesis, GeneticAdultBlack PeopleCpG IslandsDNA MethylationFemaleGenome-Wide Association StudyGhanaGlycated HemoglobinHumansMaleMendelian Randomization AnalysisMiddle AgedNigeriaQuantitative Trait LociGlycated HemoglobinDNA methylationEWASMendelian randomisationType 2 diabetesWest Africans

Identifiers

PMID42032377
PMCPMC13236806

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.