Fang Shen1, Changman Guo2, Yan Wang1, Fei Yu1, Dongdong Zhang1, Xue Liu3, Yue Ba4, Chongjian Wang3, Wenjie Li5, Xing Li6. 1. Department of Nutrition and Food Hygiene, College of Public Health, Zhengzhou University, 100 Kexue Avenue, 450001, Henan, China. 2. Shaoxing Center of Diseases for Control and Prevention, Shaoxing, 312000, Zhejiang, China. 3. Department of Epidemiology and Biostatistics, College of Public Health, Zhengzhou University, 100 Kexue Avenue, 450001, Henan, China. 4. Department of Occupational and Environmental Health Science, College of Public Health, Zhengzhou University, 100 Kexue Avenue, 450001, Henan, China. 5. Department of Nutrition and Food Hygiene, College of Public Health, Zhengzhou University, 100 Kexue Avenue, 450001, Henan, China. Lwj@zzu.edu.cn. 6. Department of Nutrition and Food Hygiene, College of Public Health, Zhengzhou University, 100 Kexue Avenue, 450001, Henan, China. 15093285830@163.com.
Abstract
BACKGROUND/ OBJECTIVES: The present cross-sectional study evaluated the association of vitamin D receptor (VDR) variants with serum 25(OH)D3 levels and their interaction on essential hypertension (EH) risk. SUBJECTS/ METHODS: 1539 patients were eligible in the study population. Two loci in VDR gene (rs2239179, rs2189480) were genotyped by TaqMan probe assays. Logistic regression, Kruskal-Wallis rank test and Chi-square test were used to determine the association among VDR polymorphisms, serum vitamin D metabolites, and the risk of EH. Interaction plots were performed to explain the interaction effects of circulating 25(OH)D3 levels and VDR variants on EH susceptibility. RESULTS: After potential confounding adjustment, we observed that the mutations of VDR (rs2239179/rs2189480) were associated with the increased risk of EH (P < 0.05). Moreover, plasma 25(OH)D3 levels were inversely associated with EH, However, we did not find the association between serum 25(OH)D3 and VDR variants. When comparing with wild-type homozygous and heterozygous genotype carriers with vitamin D sufficiency, hypovitaminosis D and insufficient participants carrying homozygous variant genotype of rs2239179 showed a higher risk of EH, increased by 113% (OR = 2.13, 95% CI: 1.20, 3.80); Notably, the detrimental effect of rs2239179 homozygous variant on EH became stronger in the case of serum 25(OH)D3 <30 ng/ml. However, we did not find the interaction effect between rs2189480 variants and serum 25(OH)D3 levels on the risk of EH. CONCLUSIONS: Our results suggested that the mutations of VDR may accelerate the progression of EH etiology, especially when suffering hypovitaminnosis D and insufficiency.
BACKGROUND/ OBJECTIVES: The present cross-sectional study evaluated the association of vitamin D receptor (VDR) variants with serum 25(OH)D3 levels and their interaction on essential hypertension (EH) risk. SUBJECTS/ METHODS: 1539 patients were eligible in the study population. Two loci in VDR gene (rs2239179, rs2189480) were genotyped by TaqMan probe assays. Logistic regression, Kruskal-Wallis rank test and Chi-square test were used to determine the association among VDR polymorphisms, serum vitamin D metabolites, and the risk of EH. Interaction plots were performed to explain the interaction effects of circulating 25(OH)D3 levels and VDR variants on EH susceptibility. RESULTS: After potential confounding adjustment, we observed that the mutations of VDR (rs2239179/rs2189480) were associated with the increased risk of EH (P < 0.05). Moreover, plasma 25(OH)D3 levels were inversely associated with EH, However, we did not find the association between serum 25(OH)D3 and VDR variants. When comparing with wild-type homozygous and heterozygous genotype carriers with vitamin D sufficiency, hypovitaminosis D and insufficient participants carrying homozygous variant genotype of rs2239179 showed a higher risk of EH, increased by 113% (OR = 2.13, 95% CI: 1.20, 3.80); Notably, the detrimental effect of rs2239179 homozygous variant on EH became stronger in the case of serum 25(OH)D3 <30 ng/ml. However, we did not find the interaction effect between rs2189480 variants and serum 25(OH)D3 levels on the risk of EH. CONCLUSIONS: Our results suggested that the mutations of VDR may accelerate the progression of EH etiology, especially when suffering hypovitaminnosis D and insufficiency.