Placenta is an extrarenal source of calcitriol and pregnancy is associated with increased maternal serum levels of this hormone. It has been reported that insulin-like growth factor I (IGF-I) stimulates placental calcitriol synthesis and that circulating levels of both hormones are low in preeclampsia. Since calcitriol production has not been determined in placental homogenates in preeclampsia, the aim of the present study was to establish if placental calcitriol synthesis and IGF-I concentration are altered in this tissue obtained from preeclamptic pregnancies. Placental samples were obtained from 8 preeclamptic (PE group) and 8 normotensive (NT group) pregnant women. Calcitriol synthesis was determined using [(3)H]-25(OH)D3 (2.94nM) as precursor and [(3)H]-1,25(OH)2D3 produced was calculated as the percentage of radioactivity co-eluting with unlabelled 1,25(OH)2D3 after two successive high pressure liquid chromatographies. Placental IGF-I levels were determined by RIA. In addition, maternal and umbilical calcitriol and IGF-I levels were also determined in these 2 groups using radioreceptor assay and RIA, respectively. The results of the present study showed that placentas from both groups were able to convert [(3)H]-25(OH)D3 into more polar metabolites. In the PE group, placental [(3)H]-1,25(OH)2D3 synthesis was significantly lower than in the NT group (19.6±6.2 vs 29.9±8.1fmoles/200mg wet weight, P=0.013). Regarding IGF-I, its levels were significantly lower in placentas of the PE group than in the NT group (15.2±3.9 vs 21.6±4.9ng/g wet weight, P=0.012). Maternal and umbilical calcitriol levels were significantly lower in the PE than in the NT group (P<0.001). In the PE group, serum IGF-I levels were significantly lower only in the maternal circulation (P<0.05). In conclusion, placental calcitriol synthesis and IGF-I levels are low in preeclampsia which may contribute to decreased local placental functions related to these two hormones and/or to decreased maternal and fetal pool of 1,25(OH)2D3 during preeclamptic pregnancies. This article is part of a Special Issue entitled '16th Vitamin D Workshop'.
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http://dx.doi.org/10.1016/j.jsbmb.2013.12.014 | DOI Listing |
Int J Mol Sci
January 2025
Department of Stem Cells and Regenerative Medicine, Institute of Natural Fibres and Medicinal Plants, Kolejowa 2, 62-064 Plewiska, Poland.
Vitamin D affects bone metabolism and calcium-phosphate metabolism. Its deficiency leads to bone mineralization disorders and is the cause of abnormal skeletal development from fetal life to the period of completed skeletal growth. In later periods of life, vitamin D deficiency leads to bone metabolism disorders, i.
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September 2024
Hospital de Niños Dr. Roberto del Río, Santiago, Chile.
Hereditary tyrosinemia type 1 (HT-1) is an inborn error of metabolism caused by a defect in tyrosine (tyr) degradation. This defect results in the accumulation of succinylacetone (SA), causing liver failure with a high risk of hepatocarcinoma and kidney injury, leading in turn to Fanconi syndrome with urine loss of phosphate and secondary hypophosphatemic rickets (HR). HT-1 diagnosis is usually made in infants with acute or chronic liver failure or by neonatal screening programs.
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January 2025
Unit of Endocrinology, Department of Translational Medicine and Surgery, Università Cattolica del Sacro Cuore, Fondazione Policlinico "A. Gemelli" IRCCS, Largo Gemelli 8, 00168 Rome, Italy.
Hypercalcemia is a frequently encountered laboratory finding in endocrinology, warranting accurate clinical and laboratory evaluation to identify its cause. While primary hyperparathyroidism and malignancies represent the most common causes, many other etiologies have been described, including some reports of hypercalcemia secondary to adrenal insufficiency. On the contrary, hypoparathyroidism is a relatively common cause of hypocalcemia, often arising as a complication of thyroid surgery.
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January 2025
Laboratório de Imunidade Natural (LIN), Instituto de Patologia Tropical e Saúde Pública, Universidade Federal de Goiás, Goiânia, Goiás, Brazil.
Background: The vitamin D pathway contributes to the microbicidal activity of macrophages against infection. In addition to induction of this pathway, interferon-gamma (IFNγ), interleukin (IL)-15, and IL32γ are part of a network of pro-inflammatory cytokines. The aim of this study was to evaluate single-nucleotide polymorphisms (SNPs) in the components of the vitamin D pathway and associated cytokine genes that could be related to resistance or susceptibility to American tegumentary leishmaniasis (ATL).
View Article and Find Full Text PDFFront Immunol
January 2025
Department of Biomedical Sciences, Faculty of Medicine and Health Sciences, An-Najah National University, Nablus, Palestine.
Background And Aim: NK cells and NK-cell-derived cytokines were shown to regulate neutrophil activation in acute lung injury (ALI). However, the extent to which ALI regulates lung tissue-resident NK (trNK) activity and their molecular phenotypic alterations are not well defined. We aimed to assess the impact of 1,25-hydroxy-vitamin-D3 [1,125(OH)D] on ALI clinical outcome in a mouse model and effects on lung trNK cell activations.
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