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E. M. CRUICKSHANK and E. KODICEK

SUMMARY

Hypervitaminosis was produced in young growing rats and the effect of daily injections of cortisone acetate (CA) was studied on growth, metastatic calcification, urinary phosphorus excretion and bone ash.

Cortisone treatment did not ameliorate the weight loss, clinical appearance, histological lesions or the increased urinary phosphorus. excretion of the hypervitaminotic rats. Control rats, treated with CA alone, showed no untoward effects at the dose levels employed.

It is concluded that cortisone does not act as a direct antimetabolite towards vitamin D. The antagonistic effect of the hormone observed in man may be due to reversal of the toxic action of vitamin D by an indirect mechanism, affecting the metabolic sites, such as intestinal tissue, kidney tubules and/or skeletal tissue, on which both vitamin D and cortisone appear to act.

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M. WINTER, E. MORAVA, and G. SIMON

SUMMARY

The effect of 20 i.u. vitamin D3 on the intestinal absorption of calcium was investigated in thyroidectomized and control rachitic rats. Vitamin D3 increased both duodenal and jejunal calcium absorption in the absence of the thyroid glands. These results suggest that neither thyroxine nor calcitonin are necessary for the effect of vitamin D3 on intestinal calcium absorption.

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Liat Abovich Gilad, Tali Bresler, Julia Gnainsky, Patricia Smirnoff, and Betty Schwartz

performed with specific anti-ERα and -ERβ antibodies. MCF-7 cells expressed both ERα and ERβ, but in HT29 cells, we detected only ERβ (Fig. 1 ). Equal loading was verified by Ponceau red staining (not shown). Effect of E2, vitamin D

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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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D R Shamley, G Veale, J M Pettifor, and R Buffenstein

Abstract

The effects of vitamin D deficiency on the ontogeny of calcium-binding proteins (CaBPs) and the vitamin D receptor (VDR) in the placenta and yolk sac of the mouse were examined. Maternal vitamin D status did not affect the time of appearance of CaBP-D9k (9 kDa) in the yolk sac endoderm or trophoblastic giant cells (TGCs) of the placenta. VDRs were undetectable in TGCs and yolk sac endoderm, but were present in the intraplacental yolk sac. Since yolk sac endoderm and TGCs contain CaBP but not VDR, it is unlikely that CaBP synthesis and/or activity in these cells is controlled by vitamin D. The TGCs, therefore, may be involved in vitamin D-independent transplacental transfer of calcium.

Journal of Endocrinology (1996) 150, 25–32

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D. Faict, P. De Moor, R. Bouillon, W. Heyns, H.-J. Heiniger, D. Corrow, and E. Lesaffre

ABSTRACT

The influence of age, sex and strain on the serum concentration of transcortin (corticosteroid-binding globulin) and vitamin D-binding protein (DBP) in mice was investigated. The effect of age was studied in two strains, C57BL/6JPfd and BALB/cmHeAPfd. The concentration of transcortin and DBP increased with age. In young animals the concentration of each protein showed a significant strain difference, which disappeared in older mice for DBP, but not for transcortin. In 7-day-old animals, no sex difference was observed for either protein, but in older animals a clear sex difference was found for transcortin. Adult males tended to have somewhat higher levels of DBP than adult females, but this difference was significant only on day 70.

The variation in transcortin and DBP levels was further investigated in a large number of mouse strains. The DBP concentration did not markedly vary among strains (5·98–9·65 μmol/l in males and 5·08–8·85 μmol/l in females). Transcortin, however, showed marked strain variations, ranging from 0·72 to 2·06 μmol/l in males and from 1·02 to 4·55 μmol/l in females and there was a significant correlation (r= 0·66, n= 26, P<0·001) between the mean transcortin levels in males and females of different strains. Interstrain variation was much higher than intrastrain variation or variation among related strains, suggesting that the transcortin concentration is largely controlled by genetically determined factors.

There was a significant correlation (r= 0·82, n = 9, P<0·01) between the mean corticosterone and transcortin concentrations (measured at 21.00 h). Consequently, differences in the free corticosterone levels in the serum of various mouse strains were smaller than the differences in the total corticosterone concentrations. The affinity of transcortin for corticosterone was similar in all but one strain; however, transcortin of the RIIIS/J strain showed a lower affinity for corticosterone.

J. Endocr. (1986) 109, 141–147

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H. Skjødt, J. A. Gallagher, J. N. Beresford, M. Couch, J. W. Poser, and R. G. G. Russell

ABSTRACT

The effects of six natural vitamin D metabolites of potential biological and therapeutic interest, 1,25-dihydroxyvitamin D3 (1,25-(OH)2D3), 25-hydroxyvitamin D3 (25-OH-D3), 24R,25-dihydroxyvitamin D3 (24R,25-(OH)2D3), 1,24R,25-trihydroxyvitamin D3 (1,24R,25-(OH)3D3), 25S,26-dihydroxyvitamin D3 (25S,26-(OH)2D3) and 1,25S,26-trihydroxyvitamin D3 (1,25S,26-(OH)3D3) on cell replication and expression of the osteoblastic phenotype in terms of osteocalcin production were examined in cultured human bone cells. At a dose of 5 × 10−12 mol/l, 1,25-(OH)2D3 stimulated cell proliferation, whereas at higher doses (5 × 10−9−5 × 10 −6 mol/l) cell growth was inhibited in a dose-dependent manner. The same pattern of effects was seen for the other metabolites in a rank order of potency: 1,25-(OH)2D3> 1,25S,26-(OH)3D3 = 1,24R,25-(OH)3D3>25S,26-(OH)2D3 = 24R,25-(OH)2D3 = 25-OH-D3. Synthesis of osteocalcin was induced by 1,25-(OH)2D3 in doses similar to those required to inhibit cell proliferation. Biphasic responses were observed for some of the metabolites in terms of osteocalcin synthesis, inhibitory effects becoming apparent at 5 × 10−6 mol/l. The cells did not secrete osteocalcin spontaneously. These results indicate that vitamin D metabolites may regulate growth and expression of differentiated functions of normal human osteoblasts.

J. Endocr. (1985) 105, 391–396

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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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T Pitcher, I N Sergeev, and R Buffenstein

Abstract

Vitamin D may be endogenously synthezised in the skin in the presence of sunlight or, alternatively, acquired from dietary sources. Cryptomys damarensis appear to have a naturally impoverished vitamin D status with low plasma concentrations of both 25-hydroxyvitamin D (25(OH)D; <5 ng/ml) and 1,25-dihydroxyvitamin D (1,25(OH)2D; <20 pg/ml). We attribute this to their underground habitat and herbivorous habits. We questioned whether these subterranean mammals could utilize sunlight-mediated pathways and therefore compared vitamin D metabolism and function when animals were (a) housed naturally (control), (b) given an oral vitamin D3 (D3) supplement (1 IU/g dry matter food eaten per day) and (c) exposed to 10 h of sunlight. Control animals exhibited a highly efficient apparent fractional absorption of both calcium (Ca) and inorganic phosphorus (Pi) (>90%), passive mode of intestinal mineral uptake, yet tightly regulated serum ionized calcium (Ca2+). The ratio of 25(OH)D-1α-hydroxylase (1-OHase) to 25(OH)D-24R-hydroxylase (24-OHase) activity in the kidney, corresponded with a state of vitamin D deficiency. Cryptomys damarensis responded to both oral D3 supplementation and sun exposure by an increase in plasma concentration of 1,25(OH)2D with a commensurate decline (P<0·05) in 1-OHase activity, and a resulting decrease (P<0·05) in the ratio of 1-OHase:24-OHase activity. Despite these changes, the intestinal mode of Ca uptake and plasma total Ca, Ca2+ and Pi remained unchanged with either treatment. Responses to sunlight were less pronounced than that of oral D3 supplementation. These data confirm that naturally vitamin D-deficient mole-rats can convert vitamin D to the active hormone 1,25(OH)2D, and indicate that mole-rats function optimally at the low concentrations of vitamin D metabolites found naturally. Furthermore, these animals exhibit a highly efficient vitamin D-independent mode of intestinal Ca absorption.

Journal of Endocrinology (1994) 143, 367–374

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N Akeno, A Matsunuma, T Maeda, T Kawane, and N Horiuchi

We investigated the effects of dexamethasone on vitamin D-1alpha-hydroxylase and -24-hydroxylase expression and on vitamin D receptor (VDR) content in the kidneys of mice fed either a normal (NCD) diet or a calcium- and vitamin D-deficient (LCD) diet for 2 weeks. For the last 5 days mice received either vehicle or dexamethasone (2 mg/kg per day s.c.). Dexamethasone significantly increased plasma calcium concentrations without changing plasma concentrations of 1,25-dihydroxyvitamin D(3) (1,25(OH)(2)D(3)) in both NCD and LCD groups. Northern blot and enzyme activity analyses in NCD mice revealed that dexamethasone increased renal VDR mRNA expression modestly and greatly increased 24-hydroxylase mRNA abundance and enzyme activity, but did not affect 1alpha-hydroxylase mRNA abundance and enzyme activity. In mice fed an LCD diet, dexamethasone increased renal VDR mRNA expression 1.5-fold, decreased 1alpha-hydroxylase mRNA abundance (52%) and activity (34%), and markedly increased 24-hydroxylase mRNA abundance (16-fold) and enzyme activity (9-fold). Dexamethasone treatment did not alter functional VDR number (B(max) 125-141 fmol/mg protein) or ligand affinity (K(d) 0.13-0.10 nM) in LCD mice. Subcutaneous injections of 1,25(OH)(2)D(3) (0.24 nmol/kg per day for 5 days) into NCD mice strongly increased renal 24-hydroxylase mRNA abundance and enzyme activity, while there was no effect of dexamethasone on renal 24-hydroxylase expression in these mice. This may be due to overwhelming induction of 24-hydroxylase by 1,25(OH)(2)D(3). These findings suggest that glucocorticoid-induced osteoporosis is caused by direct action of the steroids on bone, and the regulatory effect of glucocorticoids on renal 25-hydroxyvitamin D(3) metabolism may be less implicated in the initiation and progression of the disease.