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ABSTRACT
The effects of vitamin D3 deficiency on the ontogeny of calcium-binding proteins (CaBPs) and the vitamin D receptor in the duodenum, kidney and cerebellum of the mouse were examined. Maternal vitamin D status did not affect the time of appearance of the fetal 28 kDa CaBP (CaBP-D28k) in the cerebellum, kidney and duodenum, and the 9 kDa CaBP (CaBP-D9k) in the intestine and kidney. Vitamin D receptor was undetectable in all fetal tissues, regardless of maternal vitamin D status, at all stages of gestation examined. Thus it appears that maternal vitamin D status does not affect the ontogeny of CaBP-D9k or CaBP-D28k in the mouse fetus. The factors that influence the appearance of calbindins in the fetus are unclear.
Journal of Endocrinology (1993) 139, 473–478
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ABSTRACT
The vitamin D hormone 1,25-dihydroxyvitamin D3 (1,25(OH)2D3) is generated by a series of hydroxylation steps in the liver and kidneys. We investigated whether naturally vitamin D-deficient subterranean mammals (naked mole rats, Heterocephalus glaber) employ the same enzymatic pathways, and whether these are regulated in a similar manner to that established for other mammals.
Vitamin D3-25-hydroxylase in the liver and both 25-hydroxyvitamin D3-l-hydroxylase and 25-hydroxyvitamin D3-24 hydroxylase (1-OHase and 24-OHase) in the kidney were detectable in mole rats. As expected for vitamin D-deficient mammals, the 1-OHase activity predominated over the 24-OHase. After mole rats received a supraphysiological supplement of vitamin D3, 1-OHase activity was suppressed and 24-OHase activity was enhanced. Irrespective of vitamin D status, forskolin (a protein kinase A activator) and dibutyryl cyclic AMP did not alter the activity of either 1-OHase or 24-OHase. These findings suggest that the response of renal hydroxylases to parathyroid hormone was blunted. Phorbol esters, 12-O-tetradecanoylphorbol 13-acetate (TPA) and 1-oleoyl-2-acetylglycerol (OAG) (protein kinase C activators), suppressed 1-OHase activity. 24-OHase activity was induced by TPA but not by OAG. These effects were similar to those illicited by vitamin D3 supplementation but were additive in that they increased the responses shown in vitamin D-replete mole rats.
These data confirm that naturally vitamin D-deficient mole rats can convert vitamin D3 to the hormone, 1,25(OH)2D3. Furthermore, the enzymes 1-OHase and 24-OHase present in the kidneys of these mammals are regulated independently by 1,25(OH)2D3 and protein kinase C-mediated pathways of intracellular signalling, but are not regulated by the cyclic AMP–protein kinase A signal transduction pathway.
Journal of Endocrinology (1993) 138, 59–64
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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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ABSTRACT
The damara mole rat, Cryptomys damarensis, is a strictly subterranean dwelling herbivorous rodent that in its natural habitat has no access to any obvious source of cholecalciferol (D3). We examined the effects of D3 supplementation, at physiological and supraphysiological doses, on calcium metabolism, plasma concentrations of calcium and alkaline phosphatase (ALP) and D3 metabolites. Animals not receiving a D3 supplement maintained normal plasma calcium concentrations. In addition, they exhibited a high apparent fractional mineral absorption efficiency (91%) and maintained a positive mineral flux. The serum concentration of 25-(OH)D3 was undetectable (< 5 nmol/l) and that of 1,25-(OH)2D3 was 41±10 pmol/l. Supplementation at a physiological dose of D3 resulted in increased plasma concentrations of D3 metabolites, food intake, apparent fractional absorption efficiency and apparent fractional retention efficiency. Despite the 1·8-fold increase in food intake, body mass remained constant suggesting that the enhanced energy intake was dissipated in catabolic processes. Plasma calcium and ALP concentrations were not significantly altered with physiological doses of D3. The group given supraphysiological doses of D3 exhibited hypercalcaemia, increased creatinine concentrations and markedly increased ALP levels. These data indicate that a pathological response to D3 intoxication occurred and that hepatic and renal excretory functions were impaired. It appears, therefore, that these animals function optimally at the low concentrations of D3 metabolites found naturally. Supplementation at both physiological and supraphysiological doses of D3 may disadvantage the damara mole rat.
Journal of Endocrinology (1991) 131, 197–202