Language

English

Publication Date

10-10-2025

Journal

Nature Communications

DOI

10.1038/s41467-025-64927-5

PMID

41073432

PMCID

PMC12514310

PubMedCentral® Posted Date

10-10-2025

PubMedCentral® Full Text Version

Post-print

Abstract

Type 2 diabetes is associated with a range of non-cardiovascular non-oncologic comorbidities. To move beyond associations and evaluate causal effects between type 2 diabetes genetic predisposition and 21 comorbidities, we apply Mendelian randomization analysis using genome-wide association studies across multiple genetic ancestries. Additionally, leveraging eight mechanistic clusters of type 2 diabetes genetic profiles, each representing distinct biological pathways, we investigate causal links between cluster-stratified type 2 diabetes genetic predisposition and comorbidity risk. We identify causal effects of type 2 diabetes genetic predisposition driven by distinct genetic clusters. For example, the risk-increasing effects of type 2 diabetes genetic predisposition on cataracts and erectile dysfunction are primarily attributed to adiposity and glucose regulation mechanisms, respectively. We observe opposing effect directions across different genetic ancestries for depression, asthma and chronic obstructive pulmonary disease. Our findings leverage the heterogeneity underpinning type 2 diabetes genetic predisposition to prioritize biological mechanisms underlying causal relationships with comorbidities.

Keywords

Humans, Diabetes Mellitus, Type 2, Genetic Predisposition to Disease, Genome-Wide Association Study, Comorbidity, Mendelian Randomization Analysis, Pulmonary Disease, Chronic Obstructive, Male, Polymorphism, Single Nucleotide, Asthma, Depression, Female, Cataract, Risk Factors

Published Open-Access

yes

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