Role of Vitamin-D Receptor (VDR) single nucleotide polymorphisms in gestational hypertension development: A case-control study.
Journal
PloS one
ISSN: 1932-6203
Titre abrégé: PLoS One
Pays: United States
ID NLM: 101285081
Informations de publication
Date de publication:
2020
2020
Historique:
received:
18
06
2020
accepted:
05
09
2020
entrez:
13
11
2020
pubmed:
14
11
2020
medline:
8
1
2021
Statut:
epublish
Résumé
Recent literature data have highlighted the important role of hypovitaminosis D in pregnancy complications and prenatal/perinatal health. Vitamin D action takes place through vitamin D receptor (VDR) activation. Two single nucleotide polymorphisms of VDR gene, FokI and BsmI, have been reported to affect VDR molecular signaling and be associated with several disorders, including hypertension. We carried out a case-control study aimed to assess vitamin D serum levels together with the distribution of VDR FokI and BsmI in a population of 116 pregnant women with gestational hypertension (GH) and 69 normotensive pregnant women (CTR). Hypovitaminosis D was largely prevalent both in GH (81%) and CTR (69%) pregnant women. Vitamin D insufficiency (10-30 ng/ml) had a similar frequency in both cohorts (GH 60% vs CTR 58%), while vitamin D deficiency (<10 ng/ml) was more frequent in GH cohort than in CTR one (21% vs 11%). Regression analysis showed that GH was significantly (p = 0.031) linked to vitamin D status. Vitamin D deficiency was associated with a threefold-increased risk of developing GH, while a normal vitamin D status was protective against this pregnancy disorder. The VDR FF/bB haplotype was the most frequent in GH cohort, and resulted to increase by two folds the risk for GH. Notably, hypovitaminosis D was found in 92% of FF/bB GH pregnant women, 27% of which had deficient vitamin D levels compared with 11% of their normotensive counterparts. Despite being preliminary, these findings suggest that genotyping of pregnant women for VDR polymorphisms may be useful for a tailored vitamin D supplementation strategy.
Sections du résumé
BACKGROUND
Recent literature data have highlighted the important role of hypovitaminosis D in pregnancy complications and prenatal/perinatal health. Vitamin D action takes place through vitamin D receptor (VDR) activation. Two single nucleotide polymorphisms of VDR gene, FokI and BsmI, have been reported to affect VDR molecular signaling and be associated with several disorders, including hypertension.
METHODS
We carried out a case-control study aimed to assess vitamin D serum levels together with the distribution of VDR FokI and BsmI in a population of 116 pregnant women with gestational hypertension (GH) and 69 normotensive pregnant women (CTR).
RESULTS
Hypovitaminosis D was largely prevalent both in GH (81%) and CTR (69%) pregnant women. Vitamin D insufficiency (10-30 ng/ml) had a similar frequency in both cohorts (GH 60% vs CTR 58%), while vitamin D deficiency (<10 ng/ml) was more frequent in GH cohort than in CTR one (21% vs 11%). Regression analysis showed that GH was significantly (p = 0.031) linked to vitamin D status. Vitamin D deficiency was associated with a threefold-increased risk of developing GH, while a normal vitamin D status was protective against this pregnancy disorder. The VDR FF/bB haplotype was the most frequent in GH cohort, and resulted to increase by two folds the risk for GH. Notably, hypovitaminosis D was found in 92% of FF/bB GH pregnant women, 27% of which had deficient vitamin D levels compared with 11% of their normotensive counterparts.
CONCLUSIONS
Despite being preliminary, these findings suggest that genotyping of pregnant women for VDR polymorphisms may be useful for a tailored vitamin D supplementation strategy.
Identifiants
pubmed: 33186385
doi: 10.1371/journal.pone.0239407
pii: PONE-D-20-18772
pmc: PMC7665745
doi:
Substances chimiques
Receptors, Calcitriol
0
VDR protein, human
0
Calcifediol
P6YZ13C99Q
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
e0239407Déclaration de conflit d'intérêts
The authors have declared that no competing interests exist.
Références
Eur J Nutr. 2013 Oct;52(7):1771-9
pubmed: 23262750
Annu Rev Pathol. 2010;5:173-92
pubmed: 20078220
Clin Endocrinol (Oxf). 2011 Jun;74(6):783-90
pubmed: 21521263
Environ Health Perspect. 2003 Sep;111(12):1461-4
pubmed: 12948884
BMC Pregnancy Childbirth. 2017 Jul 15;17(1):231
pubmed: 28709403
Clin Chim Acta. 2006 Sep;371(1-2):1-12
pubmed: 16563362
Arch Gynecol Obstet. 2017 Apr;295(4):867-872
pubmed: 28243732
Front Endocrinol (Lausanne). 2018 Aug 31;9:500
pubmed: 30233496
Ci Ji Yi Xue Za Zhi. 2019 Sep 16;31(4):201-206
pubmed: 31867246
Placenta. 2008 Sep;29(9):763-71
pubmed: 18687466
Eur Rev Med Pharmacol Sci. 2019 Oct;23(20):9066-9074
pubmed: 31696497
Int J Food Sci Nutr. 2020 May;71(3):276-285
pubmed: 31928386
Am J Clin Nutr. 2016 Aug;104(2):354-61
pubmed: 27357092
J Hypertens. 2003 Nov;21(11):2069-75
pubmed: 14597850
J Steroid Biochem Mol Biol. 2004 May;89-90(1-5):387-92
pubmed: 15225806
Nurs Womens Health. 2020 Apr;24(2):91-100
pubmed: 32119830
J Matern Fetal Neonatal Med. 2016 Sep;29(18):3019-23
pubmed: 26512423
Front Endocrinol (Lausanne). 2019 Sep 10;10:563
pubmed: 31551925
Eur Rev Med Pharmacol Sci. 2017 Sep;21(18):4243-4251
pubmed: 29028072
Indian J Hum Genet. 2011 Sep;17(3):201-6
pubmed: 22345993
J Matern Fetal Neonatal Med. 2018 Mar;31(6):817-821
pubmed: 28282763
Nutrients. 2018 Mar 01;10(3):
pubmed: 29494538
J Cell Biochem. 2019 Apr;120(4):6441-6448
pubmed: 30417411
Biomed Res Int. 2015;2015:145828
pubmed: 26000281
Obstet Gynecol. 2019 Jan;133(1):e1-e25
pubmed: 30575675
Epidemiol Rev. 1997;19(2):218-32
pubmed: 9494784
Mol Biol Rep. 2012 Dec;39(12):10903-6
pubmed: 23053984
Placenta. 2011 Mar;32(3):214-21
pubmed: 21215447
Nutrients. 2020 Feb 22;12(2):
pubmed: 32098418
Int J Mol Sci. 2018 Mar 17;19(3):
pubmed: 29562608
Curr Protein Pept Sci. 2019;20(10):984-995
pubmed: 31389312
J Pregnancy. 2011;2011:123717
pubmed: 21490787
Am J Physiol Endocrinol Metab. 2012 Oct 1;303(7):E928-35
pubmed: 22871339
Biomedica. 2017 May 25;38 Suppl 1:43-53
pubmed: 29874709
Clin Biochem. 2015 Nov;48(16-17):1028-32
pubmed: 25988943
Biomed Res Int. 2015;2015:986281
pubmed: 26000308
Am J Physiol Heart Circ Physiol. 2018 Apr 1;314(4):H753-H765
pubmed: 29351464
J Steroid Biochem Mol Biol. 2020 Jul;201:105669
pubmed: 32302652
Am J Clin Nutr. 2013 Sep;98(3):787-93
pubmed: 23885046
Antioxidants (Basel). 2019 Oct 25;8(11):
pubmed: 31731439