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Detection of susceptibility loci on APOA5 and COLEC12 associated with metabolic syndrome using a genome-wide association study in a Taiwanese population

BACKGROUND: Although the association of single nucleotide polymorphisms (SNPs) with metabolic syndrome (MetS) has been reported in various populations in several genome-wide association studies (GWAS), the data is not conclusive. In this GWAS study, we assessed whether SNPs are associated with MetS...

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Autores principales: Lin, Eugene, Kuo, Po-Hsiu, Liu, Yu-Li, Yang, Albert C., Tsai, Shih-Jen
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Impact Journals LLC 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5706800/
https://www.ncbi.nlm.nih.gov/pubmed/29212154
http://dx.doi.org/10.18632/oncotarget.20967
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author Lin, Eugene
Kuo, Po-Hsiu
Liu, Yu-Li
Yang, Albert C.
Tsai, Shih-Jen
author_facet Lin, Eugene
Kuo, Po-Hsiu
Liu, Yu-Li
Yang, Albert C.
Tsai, Shih-Jen
author_sort Lin, Eugene
collection PubMed
description BACKGROUND: Although the association of single nucleotide polymorphisms (SNPs) with metabolic syndrome (MetS) has been reported in various populations in several genome-wide association studies (GWAS), the data is not conclusive. In this GWAS study, we assessed whether SNPs are associated with MetS and its individual components independently and/or through complex interactions in a Taiwanese population. METHODS: A total of 10,300 Taiwanese subjects were assessed in this study. Metabolic traits such as waist circumference, triglyceride, high-density lipoprotein (HDL) cholesterol, systolic and diastolic blood pressure, and fasting glucose were measured. RESULTS: Our data showed an association of MetS at the genome-wide significance level (P < 8.6 x 10(-8)) with two SNPs, including the rs662799 SNP in the apolipoprotein A5 (APOA5) gene and the rs16944558 SNP in the collectin subfamily member 12 (COLEC12) gene. Moreover, we identified the effect of APOA5 rs662799 on triglyceride and HDL, the effect of rs1106475 in the actin filament associated protein 1 like 2 (AFAP1L2) gene on systolic blood pressure, and the effect of rs17667932 in the mediator complex subunit 30 (MED30) gene on fasting glucose. Additionally, we found that an interaction between the APOA5 rs662799 and COLEC12 rs16944558 SNPs influenced MetS, high triglyceride, and low HDL. CONCLUSIONS: Our study indicates that the APOA5 and COLEC12 genes may contribute to the risk of MetS and its individual components independently as well as through gene-gene interactions.
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spelling pubmed-57068002017-12-05 Detection of susceptibility loci on APOA5 and COLEC12 associated with metabolic syndrome using a genome-wide association study in a Taiwanese population Lin, Eugene Kuo, Po-Hsiu Liu, Yu-Li Yang, Albert C. Tsai, Shih-Jen Oncotarget Research Paper: Pathology BACKGROUND: Although the association of single nucleotide polymorphisms (SNPs) with metabolic syndrome (MetS) has been reported in various populations in several genome-wide association studies (GWAS), the data is not conclusive. In this GWAS study, we assessed whether SNPs are associated with MetS and its individual components independently and/or through complex interactions in a Taiwanese population. METHODS: A total of 10,300 Taiwanese subjects were assessed in this study. Metabolic traits such as waist circumference, triglyceride, high-density lipoprotein (HDL) cholesterol, systolic and diastolic blood pressure, and fasting glucose were measured. RESULTS: Our data showed an association of MetS at the genome-wide significance level (P < 8.6 x 10(-8)) with two SNPs, including the rs662799 SNP in the apolipoprotein A5 (APOA5) gene and the rs16944558 SNP in the collectin subfamily member 12 (COLEC12) gene. Moreover, we identified the effect of APOA5 rs662799 on triglyceride and HDL, the effect of rs1106475 in the actin filament associated protein 1 like 2 (AFAP1L2) gene on systolic blood pressure, and the effect of rs17667932 in the mediator complex subunit 30 (MED30) gene on fasting glucose. Additionally, we found that an interaction between the APOA5 rs662799 and COLEC12 rs16944558 SNPs influenced MetS, high triglyceride, and low HDL. CONCLUSIONS: Our study indicates that the APOA5 and COLEC12 genes may contribute to the risk of MetS and its individual components independently as well as through gene-gene interactions. Impact Journals LLC 2017-09-16 /pmc/articles/PMC5706800/ /pubmed/29212154 http://dx.doi.org/10.18632/oncotarget.20967 Text en Copyright: © 2017 Lin et al. http://creativecommons.org/licenses/by/3.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0/) 3.0 (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
spellingShingle Research Paper: Pathology
Lin, Eugene
Kuo, Po-Hsiu
Liu, Yu-Li
Yang, Albert C.
Tsai, Shih-Jen
Detection of susceptibility loci on APOA5 and COLEC12 associated with metabolic syndrome using a genome-wide association study in a Taiwanese population
title Detection of susceptibility loci on APOA5 and COLEC12 associated with metabolic syndrome using a genome-wide association study in a Taiwanese population
title_full Detection of susceptibility loci on APOA5 and COLEC12 associated with metabolic syndrome using a genome-wide association study in a Taiwanese population
title_fullStr Detection of susceptibility loci on APOA5 and COLEC12 associated with metabolic syndrome using a genome-wide association study in a Taiwanese population
title_full_unstemmed Detection of susceptibility loci on APOA5 and COLEC12 associated with metabolic syndrome using a genome-wide association study in a Taiwanese population
title_short Detection of susceptibility loci on APOA5 and COLEC12 associated with metabolic syndrome using a genome-wide association study in a Taiwanese population
title_sort detection of susceptibility loci on apoa5 and colec12 associated with metabolic syndrome using a genome-wide association study in a taiwanese population
topic Research Paper: Pathology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5706800/
https://www.ncbi.nlm.nih.gov/pubmed/29212154
http://dx.doi.org/10.18632/oncotarget.20967
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