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GWAS Study

Meta-GWAS and Meta-Analysis of Exome Array Studies Do Not Reveal Genetic Determinants of Serum Hepcidin.

Galesloot TE, Verweij N, Traglia M et al.

27846281 PubMed ID
GWAS Study Type
6201 Participants
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Chapter I

Publication Details

Comprehensive information about this research publication

Authors

GT
Galesloot TE
VN
Verweij N
TM
Traglia M
BC
Barbieri C
VD
van Dijk F
GA
Geurts-Moespot AJ
GD
Girelli D
KL
Kiemeney LA
SF
Sweep FC
SM
Swertz MA
VD
van der Meer P
CC
Camaschella C
TD
Toniolo D
VS
Vermeulen SH
VD
van der Harst P
SD
Swinkels DW
Chapter II

Abstract

Summary of the research findings

Serum hepcidin concentration is regulated by iron status, inflammation, erythropoiesis and numerous other factors, but underlying processes are incompletely understood. We studied the association of common and rare single nucleotide variants (SNVs) with serum hepcidin in one Italian study and two large Dutch population-based studies. We genotyped common SNVs with genome-wide association study (GWAS) arrays and subsequently performed imputation using the 1000 Genomes reference panel. Cohort-specific GWAS were performed for log-transformed serum hepcidin, adjusted for age and gender, and results were combined in a fixed-effects meta-analysis (total N 6,096). Six top SNVs (p<5x10-6) were genotyped in 3,821 additional samples, but associations were not replicated. Furthermore, we meta-analyzed cohort-specific exome array association results of rare SNVs with serum hepcidin that were available for two of the three cohorts (total N 3,226), but no exome-wide significant signal (p<1.4x10-6) was identified. Gene-based meta-analyses revealed 19 genes that showed significant association with hepcidin. Our results suggest the absence of common SNVs and rare exonic SNVs explaining a large proportion of phenotypic variation in serum hepcidin. We recommend extension of our study once additional substantial cohorts with hepcidin measurements, GWAS and/or exome array data become available in order to increase power to identify variants that explain a smaller proportion of hepcidin variation. In addition, we encourage follow-up of the potentially interesting genes that resulted from the gene-based analysis of low-frequency and rare variants.

1495 European ancestry individuals without iron deficiency or clinical inflammation, 324 European ancestry individuals, 1206 Val Borbera (founder/genetic isolated) individuals without iron deficiency or clinical inflammation, 274 Val Borbera (founder/genetic isolated) individuals, 2,695 European ancestry individuals without iron deficiency or clinical inflammation, 207 individuals

Chapter III

Study Statistics

Key metrics and study information

6201
Total Participants
GWAS
Study Type
Yes
Replicated
1,018 European ancestry individuals, 2,876 individuals
Replication Participants
European
Ancestry
Italy, Netherlands
Recruitment Country
Chapter IV

Analysis

Comprehensive review of health and genetic findings

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Analysis In Progress

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