4.2 Article

Genetic Variants in Six-Transmembrane Epithelial Antigen of Prostate 4 Increase Risk of Developing Metabolic Syndrome in a Han Chinese Population

Journal

GENETIC TESTING AND MOLECULAR BIOMARKERS
Volume 19, Issue 12, Pages 666-672

Publisher

MARY ANN LIEBERT, INC
DOI: 10.1089/gtmb.2015.0104

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Funding

  1. Scientific Research Foundation of Jilin Provincial Health Department, China [2011Z116]

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Background: Altered expression of six-transmembrane epithelial antigen of prostate 4 (STEAP4) is linked to obesity, insulin insensitivity, metabolic homeostasis, and inflammation. This study assessed STEAP4 single nucleotide polymorphisms (SNPs) for association with a risk in developing metabolic syndrome in a Han Chinese population. Methods: A total of 3375 Han Chinese subjects were included in this case-control study with 1583 metabolic syndrome (MetS) patients and 1792 healthy controls. Four SNPs (rs1981529, rs2040657, rs10263111, rs12386756) were genotyped using polymerase chain reaction and MALDI-TOF-MS. The associations between the STAMP4 SNPs and MetS were then analyzed statistically. Results: There was no statistical difference in allele frequency of these four SNPs between the case and control populations. The genotype of rs12386756 was shown to be significantly associated with MetS (p=0.035). Compared with the AA/GG genotypes, the GA genotype of rs12386756 significantly decreased the risk of developing MetS (OR=0.77; 95% CI, 0.63-0.94; p=0.0098). There was also no haplotype that could be associated with the risk of developing MetS. Furthermore, the SNP rs1981529 of STEAP4 was associated with body-mass index, waist circumference, and systolic blood pressure, while SNP rs10263111 was associated with waist circumference and fasting glucose levels. SNP rs12386756 was associated with waist and hip circumferences. Conclusion: Some SNPs of the STEAP4 gene altered the risk of developing a metabolic syndrome in the Han Chinese population. Further studies must be conducted to understand the role of the STEAP4 gene in the pathogenesis of metabolic syndrome.

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