Low serum 25-hydroxyvitamin D levels may increase the detrimental effect of VDR variants on the risk of essential hypertension.
Eur J Clin Nutr. 2019 Dec 11. doi: 10.1038/s41430-019-0543-5.
Shen F1, Guo C2, Wang Y1, Yu F1, Zhang D1, Liu X3, Ba Y4, Wang C3, Li W5, Li X6.
Hypertension category listing contains the following
see also
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- Vitamin D Receptor
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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.
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