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Vitamin D depletion does not affect key aspects of the preeclamptic phenotype in a transgenic rodent model for preeclampsia
Ist Teil von
Journal of the American Society of Hypertension, 2016-07, Vol.10 (7), p.597-607.e1
Ort / Verlag
United States
Erscheinungsjahr
2016
Quelle
MEDLINE
Beschreibungen/Notizen
Abstract Maternal vitamin D deficiency is proposed as a risk factor for preeclampsia in humans. We tested the hypothesis that vitamin D depletion aggravates and high supplementation ameliorates the preeclampsia phenotype in an established transgenic rat model of human renin-angiotensin system (RAS) mediated preeclampsia. Methods Adult rat dams, transgenic for human angiotensinogen ( hAGT ) and mated with male rats transgenic for human renin ( hREN ), were fed either vitamin D-depleted chow (VDd) or enriched chow (VDh) two weeks before mating and during pregnancy. Mean blood pressure was recorded by tail-cuff, and 24-hour urine samples were collected in metabolic cages at days 6 and 18 of gestation. Rats were sacrificed at day 21 of gestation. Results Depleted dams (VDd) had negligible serum 25-hydroxyvitamin D2+3 levels (mean±SEM; 2.95±0.45 nmol/l vs. VDh 26.20±2.88 nmol/l, p=0.01), but in both groups, levels of 1,25(OH)2 D3 remained below detection level of 25 pmol/l. Dietary vitamin D depletion did not aggravate hypertension (mean±SEM BP, day 20 of gestation: 151.38±5.65 mmHg VDd vs. 152.00±4.10 mmHg VDh), or proteinuria. Fetal anthropometrics were similar between the groups, whereas VDd displayed lower placental:fetal weight ratios (0.15 vs. 0.16 g/g, p=0.01) and increased sFlt-1/PlGF ratio. Expression of hREN was lower in placenta of VDd dams (0.82±0.44 AU vs. 1.52±0.15 AU, p=0.04). Expression of key vitamin D metabolizing enzymes was unchanged. Conclusion Dietary vitamin D intervention did not alter key aspects of the preeclampsia phenotype using the transgenic rodent model of human RAS-mediated pre-eclampsia, plausibly due to altered vitamin D metabolism or excretion in the transgenic rats.