Vitamin D (D) deficiency during human pregnancy appears to disturb fetal growth and mineralization, but fetal development is normal in D-deficient rats and vitamin D receptor gene-ablated mice. We used the guinea pig model to investigate maternal and fetal effects of D deficiency. Pregnant (Pr) and nonpregnant (NPr) animals were fed a D-replete (+D) or D-deficient diet (-D) for 8 weeks. We further studied whether the effects of a -D diet are reversed by continuous 1,25(OH)2D3 infusion (-D+1,25) and\/or by a lactose-, Ca- and P-enriched D-deficient diet (-D+Ca\/P). Bone analyses included histomorphometry of the proximal tibiae, dual-energy X-ray absorptiometry (DXA), and quantitative computed tomography (QCT) of the femora. Depletion of 25(OH)D3 and 1,25(OH)2D3 levels and the D-deficiency syndrome were more severe in pregnant animals. Indeed, Pr\/-D but not NPr\/-D guinea pigs were hypophosphatemic, and showed robust increases in growth plate width and osteoid surface and thickness; in addition, bone mineral density on DXA was lower in Pr\/-D animals only, which was exclusively in cortical bone on QCT. Bone phenotype was partly normalized in Pr\/-D+1,25 and Pr\/-D+Ca\/P animals. Compared with +D fetuses, -D fetuses had very low or undetectable 25(OH)D3 and 1,25(OH)2D3, were hypercalcemic and hypophosphatemic, and had lower osteocalcin levels. In addition, body weight and total body bone mineral content were 10-15% lower; histomorphometry showed hypertrophic chondrocyte zone expansion and hyperosteoidosis. 1,25(OH)2D3 levels were restored in -D+1,25 fetuses, and the phenotype was partially corrected. Similarly, the fetal +D phenotype was rescued in large part in -D+Ca\/P fetuses, despite undetectable circulating 25(OH)D3 and 1,25(OH)2D3. We conclude that pregnancy markedly exacerbates D deficiency, and that augmenting Ca and P intake overrides the deleterious effects of D deficiency on fetal development.<\/p>\n","protected":false},"excerpt":{"rendered":"
Vitamin D (D) deficiency during human pregnancy appears to disturb fetal growth and mineralization, but fetal development is normal in<\/p>\n","protected":false},"author":22,"parent":0,"menu_order":0,"template":"","format":"standard","meta":{"_acf_changed":false},"tags":[],"thema":[5866,5920],"produktgruppe":[5825],"literatur_kategorie":[7223],"class_list":["post-162990","literatur","type-literatur","status-publish","format-standard","hentry","thema-diagnostics-using-leonardo-pqct","thema-pre-clinical-research","produktgruppe-pqct-en","literatur_kategorie-pre-clinical-studies"],"acf":[],"_links":{"self":[{"href":"https:\/\/stratec-med.com\/en\/wp-json\/wp\/v2\/literatur\/162990","targetHints":{"allow":["GET"]}}],"collection":[{"href":"https:\/\/stratec-med.com\/en\/wp-json\/wp\/v2\/literatur"}],"about":[{"href":"https:\/\/stratec-med.com\/en\/wp-json\/wp\/v2\/types\/literatur"}],"author":[{"embeddable":true,"href":"https:\/\/stratec-med.com\/en\/wp-json\/wp\/v2\/users\/22"}],"version-history":[{"count":0,"href":"https:\/\/stratec-med.com\/en\/wp-json\/wp\/v2\/literatur\/162990\/revisions"}],"wp:attachment":[{"href":"https:\/\/stratec-med.com\/en\/wp-json\/wp\/v2\/media?parent=162990"}],"wp:term":[{"taxonomy":"post_tag","embeddable":true,"href":"https:\/\/stratec-med.com\/en\/wp-json\/wp\/v2\/tags?post=162990"},{"taxonomy":"thema","embeddable":true,"href":"https:\/\/stratec-med.com\/en\/wp-json\/wp\/v2\/thema?post=162990"},{"taxonomy":"produktgruppe","embeddable":true,"href":"https:\/\/stratec-med.com\/en\/wp-json\/wp\/v2\/produktgruppe?post=162990"},{"taxonomy":"literatur_kategorie","embeddable":true,"href":"https:\/\/stratec-med.com\/en\/wp-json\/wp\/v2\/literatur_kategorie?post=162990"}],"curies":[{"name":"wp","href":"https:\/\/api.w.org\/{rel}","templated":true}]}}