ABSTRACT
Vitamin D is a family of steroid-hormones, derived from the diet and by de novo synthesis from 7-hydroxy-cholesterol, that plays multiple roles in human health and disease. Vitamin D is converted to 25(OH)D (25-hydroxcycholecalciferol) in the liver and to the most biologically active form, 1,25(OH)2D (calcitriol), in the kidney and other tissues, including the placenta. 1,25(OH)2D binds the intracellular vitamin D receptor, eliciting both rapid nongenomic responses and slower genomic responses. The endocrine activity of circulating 1,25(OH)2D generated by the kidney is responsible for the classic genomic actions of vitamin D in calcium metabolism and bone health. Recent work highlights the importance of the nonclassic actions of vitamin D, which result from conversion of 25(OH)D to 1,25(OH)2D in selected tissues, including the placenta, to yield autocrine and paracrine responses. These multifaceted affects include modulation of innate and adaptive immunity. The intake of vitamin D that results in adequate, insufcient, or decient, 25(OH)D levels during pregnancy is debated, but most agree that circulating 25(OH)D levels are a reasonable reection of the vitamin D status of women. Vitamin D has been assigned roles in implantation, gestational diabetes mellitus, preeclampsia, preterm birth, bacterial vaginosis, neonatal skeletal health, and the placental response to pathogens. Notably, placental trophoblasts exhibit the 1-α hydroxylase that converts 25(OH)D to active 1,25(OH)2D and the 24, 25-hydroxylase that inactivates 1,25(OH)2D. We discuss the chemistry, metabolism, and roles of vitamin D during pregnancy and in the biology of placental trophoblasts.
