Dataset Information

Analyses of shared genetic factors between asthma and obesity in children.

ABSTRACT:

Background

Epidemiologic studies consistently show associations between asthma and obesity. Shared genetics might account for this association.

Objective

We sought to identify genetic variants associated with both asthma and obesity.

Methods

On the basis of a literature search, we identified genes from (1) genome-wide association studies (GWASs) of body mass index (BMI; n = 17 genes), (2) GWASs of asthma (n = 14), and (3) candidate gene studies of BMI and asthma (n = 7). We used GWAS data from the Childhood Asthma Management Program to analyze associations between single nucleotide polymorphisms (SNPs) in these genes and asthma (n = 359 subjects) and BMI (n = 537).

Results

One top BMI GWAS SNP from the literature, rs10938397 near glucosamine-6-phosphate deaminase 2 (GNPDA2), was associated with both BMI (P = 4 x 10(-4)) and asthma (P = .03). Of the top asthma GWAS SNPs and the candidate gene SNPs, none was found to be associated with both BMI and asthma. Gene-based analyses that included all available SNPs in each gene found associations (P < .05) with both phenotypes for several genes: neuronal growth regulator 1 (NEGR1); roundabout, axon guidance receptor, homolog 1 (ROBO1); diacylglycerol kinase, gamma (DGKG); Fas apoptotic inhibitory molecule 2 (FAIM2); fat mass and obesity associated (FTO); and carbohydrate (N-acetylgalactosamine 4-0) sulfotransferase 8 (CHST8) among the BMI GWAS genes; interleukin 1 receptor-like 1 / interleukin 18 receptor 1 (IL1RL1/IL18R1), dipeptidyl-peptidase 10 (DPP10), phosphodiesterase 4D (PDE4D), V-myb myeloblastosis viral oncogene homolog (MYB), PDE10A, IL33, and especially protein tyrosine phosphatase, receptor type D (PTPRD) among the asthma GWAS genes; and protein kinase C, alpha (PRKCA) among the BMI and asthma candidate genes.

Conclusions

SNPs within several genes showed associations to BMI and asthma at a genetic level, but none of these associations were significant after correction for multiple testing. Our analysis of known candidate genes reveals some evidence for shared genetics between asthma and obesity, but other shared genetic determinants are likely to be identified in novel loci.

SUBMITTER: Melen E

PROVIDER: S-EPMC2941152 | biostudies-literature | 2010 Sep

REPOSITORIES: biostudies-literature

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Publications

Analyses of shared genetic factors between asthma and obesity in children.

Melén Erik E Himes Blanca E BE Brehm John M JM Boutaoui Nadia N Klanderman Barbara J BJ Sylvia Jody S JS Lasky-Su Jessica J

The Journal of allergy and clinical immunology 20100901 3

<h4>Background</h4>Epidemiologic studies consistently show associations between asthma and obesity. Shared genetics might account for this association.<h4>Objective</h4>We sought to identify genetic variants associated with both asthma and obesity.<h4>Methods</h4>On the basis of a literature search, we identified genes from (1) genome-wide association studies (GWASs) of body mass index (BMI; n = 17 genes), (2) GWASs of asthma (n = 14), and (3) candidate gene studies of BMI and asthma (n = 7). We ...[more]

PMID: 20816195

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Project description:Previous studies have identified differences in DNA methylation in autistic individuals compared to neurotypical individuals. Yet, it is unclear if this extends to autistic traits-subclinical manifestation of autism features in the general population. Here, we investigate the association between DNA methylation at birth (cord blood), and scores on the Social and Communication Disorders Checklist (SCDC), a measure of autistic traits, in 701 8-year-olds, by conducting a methylome-wide association study (MWAS). We did not identify significant CpGs associated with SCDC. The most significant CpG site was cg14379490, on chromosome 9 (MWAS beta?=?-?1.78?±?0.35, p value?=?5.34?×?10 -7 ). Using methylation data for autism in peripheral tissues, we did not identify a significant concordance in effect direction of CpGs with p value <?10-4 in the SCDC MWAS (binomial sign test, p value >?0.5). In contrast, using methylation data for autism from post-mortem brain tissues, we identify a significant concordance in effect direction of CpGs with a p value <?10-4 in the SCDC MWAS (binomial sign test, p value?=?0.004). Supporting this, we observe an enrichment for genes that are dysregulated in the post-mortem autism brain (one-sided Wilcoxon rank-sum test, p value?=?6.22?×?10-5). Finally, integrating genome-wide association study (GWAS) data for autism (n?=?46,350) with mQTL maps from cord-blood (n?=?771), we demonstrate that mQTLs of CpGs associated with SCDC scores at p value thresholds of 0.01 and 0.005 are significantly shifted toward lower p values in the GWAS for autism (p?<?5?×?10-3). We provide additional support for this using a GWAS of SCDC, and demonstrate a lack of enrichment in a GWAS of Alzheimer's disease. Our results highlight the shared cross-tissue methylation architecture of autism and autistic traits, and demonstrate that mQTLs associated with differences in DNA methylation associated with childhood autistic traits are enriched for common genetic variants associated with autism and autistic traits.

Dataset Information

Analyses of shared genetic factors between asthma and obesity in children.

Background

Objective

Methods

Results

Conclusions

Publications

Analyses of shared genetic factors between asthma and obesity in children.

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