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. 2021 Mar 4;13(3):837.
doi: 10.3390/nu13030837.

Vitamin D Status, Bone Mineral Density, and VDR Gene Polymorphism in a Cohort of Belarusian Postmenopausal Women

Pavel Marozik  1   2 , Alena Rudenka  3 , Katsiaryna Kobets  1 , Ema Rudenka  4
Affiliations

Vitamin D Status, Bone Mineral Density, and VDR Gene Polymorphism in a Cohort of Belarusian Postmenopausal Women

Pavel Marozik et al. Nutrients. .

Abstract

Vitamin D plays an important role in bone metabolism and is important for the prevention of multifactorial pathologies, including osteoporosis (OP). The biological action of vitamin is realized through its receptor, which is coded by the VDR gene. VDR gene polymorphism can influence individual predisposition to OP and response to vitamin D supplementation. The aim of this work was to reveal the effects of VDR gene ApaI rs7975232, BsmI rs1544410, TaqI rs731236, FokI rs2228570, and Cdx2 rs11568820 variants on bone mineral density (BMD), 25-hydroxyvitamin D level, and OP risk in Belarusian women.

Methods: The case group included 355 women with postmenopausal OP, and the control group comprised 247 women who met the inclusion criteria. TaqMan genotyping assay was used to determine VDR gene variants.

Results: Rs7975232 A/A, rs1544410 T/T, and rs731236 G/G single variants and their A-T-G haplotype showed a significant association with increased OP risk (for A-T-G, OR = 1.8, p = 0.0001) and decreased BMD (A-T-G, -0.09 g/cm2, p = 0.0001). The rs11568820 A-allele showed a protective effect on BMD (+0.22 g/cm2, p = 0.027). A significant dose effect with 25(OH)D was found for rs1544410, rs731236, and rs11568820 genotypes. Rs731236 A/A was associated with the 25(OH)D deficiency state.

Conclusion: Our novel data on the relationship between VDR gene variants and BMD, 25(OH)D level, and OP risk highlights the importance of genetic markers for personalized medicine strategy.

Keywords: VDR gene; bone mineral density; osteoporosis; polymorphism; predisposition; vitamin D.

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Conflict of interest statement

The authors declare no conflict of interest. The funders had no role in the design of the study; in the collection, analyses, or interpretation of data; in the writing of the manuscript, or in the decision to publish the results.

Figures

Figure 1
Figure 1
Linkage disequilibrium (LD) plot for rs7975232, rs1544410, rs731236, rs2228570, and rs11568820 variants of the VDR gene. LD is displayed as pairwise D’ values multiplied by 100 and given for each SNV combination within each cell. Red cells correspond to a very strong LD; rs7975232, rs1544410, and rs731236 variants are in the same LD block.
Figure 2
Figure 2
Lumbar spine (LS) BMD level in relation to VDR gene variants rs7975232 (A), rs1544410 (B), rs731236 (C), rs2228570 (D), rs11568820 (E), and rs7975232, rs1544410, and rs731236 haplotypes (F). For rs7975232, rs1544410, rs731236, and rs11568820 variants, gene/dose dependence was revealed. The rs11568820 was the only VDR gene variant with protective effect. p-values corrected for multiple testing using the FDR, β is the difference compared to the reference value. The data are presented as β (95% CI).
Figure 3
Figure 3
The association of serum 25-hydroxyvitamin D levels with VDR gene variants rs7975232 (A), rs1544410 (B), rs731236 (C), rs2228570 (D), rs11568820 (E), and rs731236 genotype distribution in groups based on Vitamin D status (F). For rs1544410, rs731236, and rs11568820 variants, gene/dose dependence was revealed. The rs11568820 was the only VDR gene variant with protective effect. p-values corrected for multiple testing using the FDR, β is the difference compared to the reference value. The data are presented as β (95% CI). * Dominant model of inheritance.
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