Bidirectional Mendelian Randomization and Multiphenotype GWAS Show Causality and Shared Pathophysiology Between Depression and Type 2 Diabetes.


Journal

Diabetes care
ISSN: 1935-5548
Titre abrégé: Diabetes Care
Pays: United States
ID NLM: 7805975

Informations de publication

Date de publication:
01 09 2023
Historique:
received: 07 12 2022
accepted: 21 06 2023
medline: 28 8 2023
pubmed: 26 7 2023
entrez: 26 7 2023
Statut: ppublish

Résumé

Depression is a common comorbidity of type 2 diabetes. We assessed the causal relationships and shared genetics between them. We applied two-sample, bidirectional Mendelian randomization (MR) to assess causality between type 2 diabetes and depression. We investigated potential mediation using two-step MR. To identify shared genetics, we performed 1) genome-wide association studies (GWAS) separately and 2) multiphenotype GWAS (MP-GWAS) of type 2 diabetes (19,344 case subjects, 463,641 control subjects) and depression using major depressive disorder (MDD) (5,262 case subjects, 86,275 control subjects) and self-reported depressive symptoms (n = 153,079) in the UK Biobank. We analyzed expression quantitative trait locus (eQTL) data from public databases to identify target genes in relevant tissues. MR demonstrated a significant causal effect of depression on type 2 diabetes (odds ratio 1.26 [95% CI 1.11-1.44], P = 5.46 × 10-4) but not in the reverse direction. Mediation analysis indicated that 36.5% (12.4-57.6%, P = 0.0499) of the effect from depression on type 2 diabetes was mediated by BMI. GWAS of type 2 diabetes and depressive symptoms did not identify shared loci. MP-GWAS identified seven shared loci mapped to TCF7L2, CDKAL1, IGF2BP2, SPRY2, CCND2-AS1, IRS1, CDKN2B-AS1. MDD has not brought any significant association in either GWAS or MP-GWAS. Most MP-GWAS loci had an eQTL, including single nucleotide polymorphisms implicating the cell cycle gene CCND2 in pancreatic islets and brain and the insulin signaling gene IRS1 in adipose tissue, suggesting a multitissue and pleiotropic underlying mechanism. Our results highlight the importance to prevent type 2 diabetes at the onset of depressive symptoms and the need to maintain a healthy weight in the context of its effect on depression and type 2 diabetes comorbidity.

Identifiants

pubmed: 37494602
pii: 153440
doi: 10.2337/dc22-2373
pmc: PMC10465984
doi:

Substances chimiques

SPRY2 protein, human 0
Membrane Proteins 0
Intracellular Signaling Peptides and Proteins 0
IGF2BP2 protein, human 0
RNA-Binding Proteins 0

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

1707-1714

Subventions

Organisme : Diabetes UK
ID : 20/0006307
Pays : United Kingdom

Informations de copyright

© 2023 by the American Diabetes Association.

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Auteurs

Jared G Maina (JG)

INSERM UMR 1283, CNRS UMR 8199, European Genomic Institute for Diabetes (EGID), Institut Pasteur de Lille, Lille, France.
University of Lille, Lille University Hospital, Lille, France.

Zhanna Balkhiyarova (Z)

Department of Clinical and Experimental Medicine, University of Surrey, Guildford, U.K.
Department of Metabolism, Digestion and Reproduction, Imperial College London, London, U.K.
People-Centred Artificial Intelligence Institute, University of Surrey, Guildford, U.K.

Arie Nouwen (A)

Department of Psychology, Middlesex University, London, U.K.

Igor Pupko (I)

Department of Clinical and Experimental Medicine, University of Surrey, Guildford, U.K.
Department of Metabolism, Digestion and Reproduction, Imperial College London, London, U.K.

Anna Ulrich (A)

Department of Metabolism, Digestion and Reproduction, Imperial College London, London, U.K.

Mathilde Boissel (M)

INSERM UMR 1283, CNRS UMR 8199, European Genomic Institute for Diabetes (EGID), Institut Pasteur de Lille, Lille, France.
University of Lille, Lille University Hospital, Lille, France.

Amélie Bonnefond (A)

INSERM UMR 1283, CNRS UMR 8199, European Genomic Institute for Diabetes (EGID), Institut Pasteur de Lille, Lille, France.
University of Lille, Lille University Hospital, Lille, France.
Department of Metabolism, Digestion and Reproduction, Imperial College London, London, U.K.

Philippe Froguel (P)

INSERM UMR 1283, CNRS UMR 8199, European Genomic Institute for Diabetes (EGID), Institut Pasteur de Lille, Lille, France.
University of Lille, Lille University Hospital, Lille, France.
Department of Metabolism, Digestion and Reproduction, Imperial College London, London, U.K.

Amna Khamis (A)

INSERM UMR 1283, CNRS UMR 8199, European Genomic Institute for Diabetes (EGID), Institut Pasteur de Lille, Lille, France.
University of Lille, Lille University Hospital, Lille, France.
Department of Metabolism, Digestion and Reproduction, Imperial College London, London, U.K.

Inga Prokopenko (I)

INSERM UMR 1283, CNRS UMR 8199, European Genomic Institute for Diabetes (EGID), Institut Pasteur de Lille, Lille, France.
University of Lille, Lille University Hospital, Lille, France.
Department of Clinical and Experimental Medicine, University of Surrey, Guildford, U.K.
People-Centred Artificial Intelligence Institute, University of Surrey, Guildford, U.K.

Marika Kaakinen (M)

Department of Clinical and Experimental Medicine, University of Surrey, Guildford, U.K.
Department of Metabolism, Digestion and Reproduction, Imperial College London, London, U.K.
People-Centred Artificial Intelligence Institute, University of Surrey, Guildford, U.K.

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