ArticlePloS one2020
Smoking-by-genotype interaction in type 2 diabetes risk and fasting glucose.
Article in PloS one, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers, 2 of them syntheses that pooled it.
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Who cites it
9 citing papers in PubMed, 2 syntheses or guidelines pooled it, 45 citations in OpenAlex.
- Effect of TCF7L2 on the relationship between lifestyle factors and glycemic parameters: a systematic review.Nutrition journal · 2022Pooled it
- Lifestyle Risk Score: handling missingness of individual lifestyle components in meta-analysis of gene-by-lifestyle interactions.European journal of human genetics : EJHG · 2021Pooled it
- Polygenic risk score for type 2 diabetes shows context-dependent effects across populations.Nature communications · 2025Article
- Identification of gene-sex hormone interactions associated with type 2 diabetes among men and women.PLoS genetics · 2025Article
- Type 2 Diabetes Polygenic Risk Score Interactions with Lifestyle Risk Factors in Black Americans.Lifestyle genomics · 2025Article
- Genetic risk scores: are they important for diabetes management? results from multiple cross-sectional studies.Diabetology & metabolic syndrome · 2023Article
- Genes, environment, and African ancestry in cardiometabolic disorders.Trends in endocrinology and metabolism: TEM · 2023Review
- Leveraging family history in genetic association analyses of binary traits.BMC genomics · 2022Article
- Interactive Effect ofDiabetes, metabolic syndrome and obesity : targets and therapy · 2020Article
Corrections and comments
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Authors and funding
58 authors at 20 institutions in 5 countries.
Funding
Abstract
Smoking is a potentially causal behavioral risk factor for type 2 diabetes (T2D), but not all smokers develop T2D. It is unknown whether genetic factors partially explain this variation. We performed genome-environment-wide interaction studies to identify loci exhibiting potential interaction with baseline smoking status (ever vs. never) on incident T2D and fasting glucose (FG). Analyses were performed in participants of European (EA) and African ancestry (AA) separately. Discovery analyses were conducted using genotype data from the 50,000-single-nucleotide polymorphism (SNP) ITMAT-Broad-CARe (IBC) array in 5 cohorts from from the Candidate Gene Association Resource Consortium (n = 23,189). Replication was performed in up to 16 studies from the Cohorts for Heart Aging Research in Genomic Epidemiology Consortium (n = 74,584). In meta-analysis of discovery and replication estimates, 5 SNPs met at least one criterion for potential interaction with smoking on incident T2D at p<1x10-7 (adjusted for multiple hypothesis-testing with the IBC array). Two SNPs had significant joint effects in the overall model and significant main effects only in one smoking stratum: rs140637 (FBN1) in AA individuals had a significant main effect only among smokers, and rs1444261 (closest gene C2orf63) in EA individuals had a significant main effect only among nonsmokers. Three additional SNPs were identified as having potential interaction by exhibiting a significant main effects only in smokers: rs1801232 (CUBN) in AA individuals, rs12243326 (TCF7L2) in EA individuals, and rs4132670 (TCF7L2) in EA individuals. No SNP met significance for potential interaction with smoking on baseline FG. The identification of these loci provides evidence for genetic interactions with smoking exposure that may explain some of the heterogeneity in the association between smoking and T2D.
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