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L. Cancela, N. Le Boulch, and L. Miravet

ABSTRACT

This work was designed to study the effect of the vitamin D content of human milk on the vitamin D status of exclusively breast-fed infants, and the relation between milk and maternal serum concentrations of vitamin D during the first month of lactation. Serum levels of calcium (Ca), phosphorus (P), magnesium (Mg) and 25-hydroxyvitamin D (25-OH-D) were determined in a racially heterogenous population of nursing women, between days 3 and 5 (L3), 15 and 18 (L15) and 30 and 45 (L30) post partum. The same parameters were determined in the serum of 1-month-old breast-fed infants. Maternal milk samples were obtained at L3, L15 and L30 and analysed for Ca, P, Mg, vitamin D and 25-OH-D content. Milk levels of Ca, P and Mg were found to be within the range previously described by other authors. No correlation was found between serum and milk levels of vitamin D and 25-OH-D in nursing mothers. The 25-OH-D concentration in milk was related to its vitamin D content and strongly correlated (P < 0·001) with the 25-OH-D levels in the serum of exclusively breast-fed infants. No significant changes were observed in maternal serum levels of 1,25-dihydroxyvitamin D (1,25-(OH)2D3) measured at L3 and L30, or between maternal and infant levels of 1,25-(OH)2D3 at L30. This study emphasizes the importance of the 25-OH-D content of maternal milk, in being primarily responsible for the vitamin D concentrations found in the serum of exclusively breast-fed infants. In contrast, serum levels of 1,25-(OH)2D3 measured in the breast-fed baby seemed mainly related to its calcaemia.

J. Endocr. (1986) 110, 43–50

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L. Cancela, P. J. Marie, N. Le Boulch, and L. Miravet

ABSTRACT

Mineral, hormonal and skeletal changes were determined in vitamin D-deficient (−D) and vitamin Dreplete (+D) mother rats and in their litters on day 20 of lactation. These results were compared with those obtained in −D mothers and pups, after giving the mothers an oral supplement (10 i.u. vitamin D3/day) during the period of lactation (20 days). Compared to +D animals, both −D lactating mothers and their pups exhibited extremely low plasma levels of 25-hydroxyvitamin D3 (25-OH-D3), diminished 1,25-dihydroxyvitamin D3 (1,25(OH)2D3) and increased levels of immunoreactive parathyroid hormone (iPTH). Vitamin D-deficient mothers also had higher levels of calcitonin and lower levels of prolactin than +D mothers. All − D animals (mothers and pups) showed increased osteoclastic bone resorption and severe osteomalacia as shown by decreased bone ash, decreased calcification rate and increased endosteal osteoid surface, volume and thickness. In mothers treated with vitamin D3 during lactation, nearly all the plasma variables measured, as well as bone histomorphometric features, were normal. In contrast, their pups still showed rickets and osteomalacia, despite normal levels of 25-OH-D3 and calcium in the plasma. These pups had raised plasma levels of 1,25(OH)2D3 and iPTH associated with persistent stimulation of bone resorption. This study showed that (1) severe vitamin D deficiency in lactating rats produced marked osteomalacia and secondary hyperparathyroidism in both mothers and pups, and (2) vitamin D treatment of − D mother rats during lactation (10 i.u. vitamin D3/day) reversed the mineral, hormonal and skeletal abnormalities in mothers but not in pups.

J. Endocr. (1985) 105, 303–309

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C. Rebut-Bonneton, J. Demignon, B. Amor, and L. Miravet

Fetal bone resorption was measured by an organ culture technique using fetuses from intact or thyroparathyroidectomized pregnant rats. These experiments were performed to investigate the effects of 1,25-dihydroxycholecalciferol (1,25-DHCC) and salmon calcitonin (SCT) in pregnant rats, on both fetal growth and fetal bone resorption.

Pregnant rats were given 0·1–0·5 μg 1,25-DHCC per day from day 17 of gestation: in intact rats bone resorption was increased and fetal growth decreased; 1,25-DHCC probably modified fetal bone resorption in the absence of fetal parathyroid secretion.

Infusion of SCT in minipumps (30 mu./h) did not modify plasma calcium levels in either the mother or fetuses, neither was bone resorption altered. In 1,25-DHCC-treated rats, SCT infusion resulted in an increase in fetal weight and a decrease in fetal bone resorption. On the other hand, SCT infusion was found to facilitate phosphate accumulation in fetuses.

At the end of the SCT infusion the SCT concentration was 450 ng/l in maternal plasma and 553± 60 ng/l in fetal plasma. Salmon calcitonin was shown to cross the placental barrier in the rats; it may interact with the effects of 1,25-DHCC in the fetus.