The role of vitamin D in regulating placental transport of calcium and phosphate in pigs was studied using the "Hannover Pig Strain" which suffers from pseudo-vitamin D-deficiency rickets, type I. Sows and fetuses of normal phenotype (heterozygotes) and of homozygote phenotype which suffered from clinical symptoms of rickets were used. The homozygote animals are devoid of renal 25-cholecalciferol-1-hydroxylase. In the rachitic sows which normally depend on treatment with pharmacological doses of vitamin D3 at intervals of four to six weeks, vitamin D-treatment was discontinued two months before conception. Ca, P and 1.25-(OH)2D3 concentrations in plasma of sows and fetuses (Aa. umb., V. umb.) were measured in samples obtained at term during cesarian section. Mean concentrations of Ca and P in heterozygote sows at parturition were 2.34 mmol/l and 2.33 mmol/l, respectively, and were significantly higher than in homozygote sows, 1.58 mmol/l and 1.26 mmol/l, respectively. Ca concentrations in plasma of the umbilical vein of fetuses from both homozygote and heterozygote sows were normal, however, (3.23 mmol/l and 2.96 mmol/l, respectively) and statistically not different from each other. No significantly different P concentrations in arterial plasma of fetuses from heterozygote or homozygote sows were seen, either. The concentrations of Ca and P in the arterial umbilical plasma were significantly higher (p less than 0.001) than in venous plasma of both homozygote and heterozygote fetuses, indicating net placental transfer of these elements in both genotypes. The concentration of 1.25-(OH)2D3 in hypocalcemic sows at term (25.5 +/- 8.25 pg/ml) was significantly lower than that in the normocalcemic (heterozygote) sows (84.1 +/- 25.6 pg/ml). The 1.25-(OH)2D3 concentration in arterial plasma of fetuses from homozygote sows was only 46% that of fetuses from normocalcemic sows which showed transfer of calcitriol from mother to fetus. It is concluded from these studies that in pigs, renal production and physiological concentrations of 1.25-(OH)2D3 in either mother or fetus is not essential for the maintainance of the Ca and P homeostasis in the fetal-maternal system.
The role of vitamin D for intestinal absorption of Ca was studied in neonatal piglets. Piglets of normal phenotype (heterozygotes) and piglets which suffered from pseudo-vitamin D deficiency rickets, type I, which were devoid of renal 25-cholecalciferol-1-hydroxylase were used for the experiments. Intestinal absorption of Ca was measured after an oral dose of 3–7 MBq 45CaCl2· Intestinal absorption of Ca was the same in heterozygotes and homozygotic rachitic piglets during the first 3–4 weeks of life. Ca absorption began to decline in rachitic piglets at the age of 4 weeks. In 8-week-old rachitic piglets intestinal Ca absorption was 50% of control piglets. Body weights of heterozygotes and rachitic piglets were the same at birth and no different weight gains were seen between the two groups during the first 4–5 weeks of life. No differences were observed during the first weeks of life in the concentrations of plasma Ca, inorganic-phosphate and alkaline-phosphatase activity between the groups. Hypocalcemia and hypophosphatemia developed in rachitic piglets between the 3rd and 5th weeks of life. Concentrations of 1,25-(OH)2D3 in plasma declined in heterozygote piglets from 130 ± 26 to 88 ± 19 pg/ml and in rachitic piglets from 67 ± 37 to 23 ± 11 pg/ml during the first 6 weeks. An intestinal nuclear 1,25-(OH)2D3 receptor was absent in neonatal piglets of both experimental groups. It is concluded that intestinal absorption of Ca in piglets during the first 2–4 weeks of life is independent of vitamin D.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.