| Literature DB >> 28757204 |
Despoina Manousaki1, Tom Dudding2, Simon Haworth2, Yi-Hsiang Hsu3, Ching-Ti Liu4, Carolina Medina-Gómez5, Trudy Voortman6, Nathalie van der Velde7, Håkan Melhus8, Cassianne Robinson-Cohen9, Diana L Cousminer10, Maria Nethander11, Liesbeth Vandenput12, Raymond Noordam13, Vincenzo Forgetta1, Celia M T Greenwood14, Mary L Biggs15, Bruce M Psaty16, Jerome I Rotter17, Babette S Zemel18, Jonathan A Mitchell18, Bruce Taylor19, Mattias Lorentzon20, Magnus Karlsson21, Vincent V W Jaddoe6, Henning Tiemeier22, Natalia Campos-Obando23, Oscar H Franco24, Andre G Utterlinden5, Linda Broer23, Natasja M van Schoor25, Annelies C Ham23, M Arfan Ikram26, David Karasik27, Renée de Mutsert28, Frits R Rosendaal28, Martin den Heijer29, Thomas J Wang30, Lars Lind8, Eric S Orwoll31, Dennis O Mook-Kanamori32, Karl Michaëlsson33, Bryan Kestenbaum9, Claes Ohlsson12, Dan Mellström34, Lisette C P G M de Groot35, Struan F A Grant36, Douglas P Kiel37, M Carola Zillikens23, Fernando Rivadeneira5, Stephen Sawcer38, Nicholas J Timpson2, J Brent Richards39.
Abstract
Vitamin D insufficiency is common, correctable, and influenced by genetic factors, and it has been associated with risk of several diseases. We sought to identify low-frequency genetic variants that strongly increase the risk of vitamin D insufficiency and tested their effect on risk of multiple sclerosis, a disease influenced by low vitamin D concentrations. We used whole-genome sequencing data from 2,619 individuals through the UK10K program and deep-imputation data from 39,655 individuals genotyped genome-wide. Meta-analysis of the summary statistics from 19 cohorts identified in CYP2R1 the low-frequency (minor allele frequency = 2.5%) synonymous coding variant g.14900931G>A (p.Asp120Asp) (rs117913124[A]), which conferred a large effect on 25-hydroxyvitamin D (25OHD) levels (-0.43 SD of standardized natural log-transformed 25OHD per A allele; p value = 1.5 × 10-88). The effect on 25OHD was four times larger and independent of the effect of a previously described common variant near CYP2R1. By analyzing 8,711 individuals, we showed that heterozygote carriers of this low-frequency variant have an increased risk of vitamin D insufficiency (odds ratio [OR] = 2.2, 95% confidence interval [CI] = 1.78-2.78, p = 1.26 × 10-12). Individuals carrying one copy of this variant also had increased odds of multiple sclerosis (OR = 1.4, 95% CI = 1.19-1.64, p = 2.63 × 10-5) in a sample of 5,927 case and 5,599 control subjects. In conclusion, we describe a low-frequency CYP2R1 coding variant that exerts the largest effect upon 25OHD levels identified to date in the general European population and implicates vitamin D in the etiology of multiple sclerosis.Entities:
Keywords: GWAS; low-frequency genetic variants; multiple sclerosis; vitamin D
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Year: 2017 PMID: 28757204 PMCID: PMC5544392 DOI: 10.1016/j.ajhg.2017.06.014
Source DB: PubMed Journal: Am J Hum Genet ISSN: 0002-9297 Impact factor: 11.043