ArticleGenome medicine2026
GWAS-by-subtraction reveals new genetic architecture and health implications of type 2 diabetes-independent gestational diabetes mellitus.
Article in Genome medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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.
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.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors.
Funding
Abstract
backgroundThe etiology of gestational diabetes mellitus (GDM) is constituted by both type 2 diabetes (T2D)-dependent and T2D-independent mechanisms. However, existing studies have evaluated the impact of T2D-dependent loci only for GDM, which limits the power to assess to what extent genetic variants or biological pathways are specific to GDM.
methodsWe subtracted the genetic effects of a genome-wide association study (GWAS) data for T2D from a GWAS data for GDM to reveal loci linked with T2D-independent components of GDM using genomic structural equation model (SEM). In the discovery stage of GWAS-by-subtraction, we used GWAS summary statistics of GDM and T2D from the FinnGen study as input latent variables (16,802 GDM cases and 237,816 controls; 71,728 T2D cases and 369,007 controls). In the replication stage, we adopted the summary statistics from a previously reported GWAS for GDM and T2D as input (21,263 GDM cases and 301,918 controls; 50,409 T2D cases and 523,897 controls). We functionally annotated variants with genome-wide significance, and performed comprehensive analyses including transcriptome-wide and proteome-wide associations, summary-data-based mendelian randomization, linkage disequilibrium score regression, and Mendelian randomization, to explore genetic patterns for T2D-dependent and -independent components of GDM.
resultsWe found 69 independent genome-wide significant loci associated with the T2D-independent components of GDM for discovery stage, of which 49 SNPs are not significant in the GWAS for GDM used as input. T2D-independent components of GDM showed only genetic correlation with birth weight dependent on maternal genetic effect (rg = 0.19; P = 0.01), whilst T2D-dependent components of GDM showed genetic correlation with birth weight dependent on fetal genetic effect (rg = -0.22; P = 4.76 × 10
conclusionsWe identified independent genetic components, loci and genes of GDM that may have been previously masked by T2D, providing more accurate targets for early detection and management of GDM.
Indexed as
Identifiers
What Socratic holds
Registered trials
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 Socratic graph.