ArticleJournal of human genetics2019
Identification of novel genetic variants for type 2 diabetes, childhood obesity, and their pleiotropic loci.
Article in Journal of human genetics, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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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.
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Who cites it
5 citing papers in PubMed, 7 citations in OpenAlex.
- An Epigenomic Meta-Analysis of Differentially Methylated Sites in Pre- and Post-Metabolic/Bariatric Surgery Adult Female Patients.Epigenomes · 2025Review
- Article
- The Potential of Albuminuria as a Biomarker of Diabetic Complications.Cardiovascular drugs and therapy · 2021Review
- High-Throughput Screening of Mouse Gene Knockouts Identifies Established and Novel High Body Fat Phenotypes.Diabetes, metabolic syndrome and obesity : targets and therapy · 2021Article
- No correlation between the variants of exostosin 2 gene and type 2 diabetes in Burkina Faso population.Journal of public health in Africa · 2020Article
Corrections and comments
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Authors and funding
7 authors at 5 institutions in 2 countries.
Funding
Abstract
Obesity has result in increased prevalence of type 2 diabetes (T2D) in children. The genetic mechanisms underlying their relationship, however, are not fully understood. Here, we aim to identify novel SNPs associated with T2D and childhood obesity (CO), especially their pleiotropic loci. We integrated the summary statistics for two independent GWASs of T2D (n = 149,821) and childhood body mass index (CBMI) (n = 35,668) using the pleiotropy-informed conditional false discovery rate (cFDR) method. By leveraging the information of different levels of association for CBMI, we observed a strong enrichment of genetic variants associated with T2D. We identified 139 T2D-associated SNPs with 125 novel ones (cFDR < 0.05). Conditioned on T2D, we identified 37 significant SNPs for CBMI (cFDR < 0.05), including 25 novel ones. The conjunctional cFDR (ccFDR) analysis showed ten novel pleiotropic loci for T2D and CBMI (ccFDR < 0.05). Interestingly, the novel SNP rs1996023 is located at protein coding gene GNPDA2 (ccFDR = 1.28E-02), which has been reported to influence the risk of T2D and CO through central nervous system. Our findings may help to explain a greater proportion of the heritability for human traits and advance the understanding of the common pathophysiology between T2D and CO.
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