Bidirectional Mendelian randomization and multiphenotype GWAS show causality and shared pathophysiology between depression and type 2 diabetes

Article

Maina, J., Balkhiyarova, Z., Nouwen, A., Pupko, I., Ulrich, A., Boissel, M., Bonnefond, A., Froguel, P., Khamis, A., Prokopenko, I. and Kaakinen, M. 2023. Bidirectional Mendelian randomization and multiphenotype GWAS show causality and shared pathophysiology between depression and type 2 diabetes. Diabetes Care. 46 (9), pp. 1707-1714. https://doi.org/10.2337/dc22-2373
TypeArticle
TitleBidirectional Mendelian randomization and multiphenotype GWAS show causality and shared pathophysiology between depression and type 2 diabetes
AuthorsMaina, J., Balkhiyarova, Z., Nouwen, A., Pupko, I., Ulrich, A., Boissel, M., Bonnefond, A., Froguel, P., Khamis, A., Prokopenko, I. and Kaakinen, M.
Abstract

OBJECTIVE
Depression is a common comorbidity of type 2 diabetes. We assessed the causal relationships and shared genetics between them.

RESEARCH DESIGN AND METHODS
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.

RESULTS
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.

CONCLUSIONS
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.

Sustainable Development Goals3 Good health and well-being
Middlesex University ThemeHealth & Wellbeing
PublisherAmerican Diabetes Association (ADA)
JournalDiabetes Care
ISSN0149-5992
Electronic1935-5548
Publication dates
Online26 Jul 2023
PrintSep 2023
Publication process dates
Submitted07 Dec 2022
Accepted21 Jun 2023
Deposited15 Dec 2025
Output statusPublished
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Open
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Supplemental file
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Additional information

The published version of the paper is available as free access on the publisher's website at http://doi.org/10.2337/dc22-2373

This Accepted Manuscript is made available with permission of the publisher as per their website: https://diabetesjournals.org/journals/pages/ada-journal-policies#cop...

Digital Object Identifier (DOI)https://doi.org/10.2337/dc22-2373
PubMed ID37494602
Web of Science identifierWOS:001166849900001
LanguageEnglish
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