Expressive

rs10927823 - DDI2

Magnitude 2.2 · 2 studies on file

Reported associations

  • Using human genetics to understand the phenotypic association between chronotype and breast cancer. - Journal of sleep research (2024) · Wu X, Yang C, Zou Y, Jones SE, Zhao X, Zhang L, Han Z, Hao Y, Xiao J, Xiao C, Zhang W, Yan P, Cui H, Tang M, Wang Y, Chen L, Zhang L, Yao Y, Liu Z, Li J, Jiang X, Zhang B · PubMed 37380357

    Little is known regarding the shared genetic influences underlying the observed phenotypic association between chronotype and breast cancer in women. Leveraging summary statistics from the hitherto largest genome-wide association study conducted in each trait, we investigated the genetic correlation, pleiotropic loci, and causal relationship of chronotype with overall breast cancer, and with its subtypes defined by the status of oestrogen receptor. We identified a negative genomic correlation between chronotype and overall breast cancer ( = -0.06, p = 3.00 × 10 ), consistent across oestrogen receptor-positive ( = -0.05, p = 3.30 × 10 ) and oestrogen receptor-negative subtypes ( = -0.05, p = 1.11 × 10 ). Five specific genomic regions were further identified

  • Genetic evidence that high BMI in childhood has a protective effect on intermediate diabetes traits, including measures of insulin sensitivity and secretion, after accounting for BMI in adulthood - Unknown journal (n.d.) · Unknown authors · PubMed 37280435

    ABSTRACT: Aims/hypothesis Determining how high BMI at different time points influences the risk of developing type 2 diabetes and affects insulin secretion and insulin sensitivity is critical. Methods By estimating childhood BMI in 441,761 individuals in the UK Biobank, we identified which genetic variants had larger effects on adulthood BMI than on childhood BMI, and vice versa. All genome-wide significant genetic variants were then used to separate the independent genetic effects of high childhood BMI from those of high adulthood BMI on the risk of type 2 diabetes and insulin-related phenotypes using Mendelian randomisation. We performed two-sample MR using external studies of type 2 diabetes, and oral and intravenous measures of insulin secretion and sensitivity. Results We found tha

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