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Biomedical subjects

S Edelstein

Publications and source records attributed to S Edelstein.

At least 73 records · Page 4Linked to original sources
PubMed1980

End-organ resistance to 1,25-dihydroxycholecalciferol.

A 13-year-old girl with total alopecia who in infancy had rickets unresponsive to large doses of vitamin D2 is described. She had profound hypocalcaemia which was resistant to treatment with high doses of dihydrotachysterol, 1 alpha-hydroxycholecalciferol, and 1,25-dihydroxycholecalciferol. Serum concentrations of 25-hydroxyvitamin D were normal but those of 1,25-dihydroxycholecalciferol were markedly raised (674 and 745 pg/ml). In addition, 24,25-dihydroxyvitamin D was undetectable in serum. Administration of synthetic 24,25-dihydroxycholecalciferol was followed by normocalcaemia which persisted long after treatment was stopped. Her sister, who died at the age of 10 months, also had had total alopecia, rickets, and hypocalcaemia resistant to vitamin-D2 therapy. In this familial syndrome there seems to be end-organ resistance to the action of 1,25-dihydroxycholecalciferol, possibly as a result of changes at the receptor sites.

Adolescent↗
PubMed1980

Absorption and excretion of cholecalciferol and of 25-hydroxycholecalciferol and metabolites in birds.

The absorption and excretion in vivo of cholecalciferol or 25-hydroxycholecalciferol (25-HCC) were determined in chicks (Gallus domesticus) and turkeys (Meleagris gallopavo). The overall net cholecalciferol or 25-HCC absorption in chicks and cholecalciferol in turkey poults was 66.5 +/- 3.3, 74.9 +/- 3.7 and 83.6 +/- 7.1% of the intake, respectively. The absorption of cholecalciferol or 25-HCC in chicks and turkeys occurred at the upper part of the intestine. 25-HCC, esters and non-polar metabolites of cholecalciferol or 25-HCC, and their polar metabolites, were secreted in the duodenum of chicks and turkeys but were partially reabsorbed at the upper part of the jejunum.

Animals↗
PubMed1979

Metabolism of cholecalciferol in land snails.

1. Radioactively labelled cholecalciferol was injected into the land snails Levantina hiersolyma and Theba pisana. Three metabolites (C, D and E), more polar than cholecalciferol, were found. 2. Metabolite C was found to be identical with 25-hydroxycholecalciferol. On injection of 25-hydroxy[26,27-3H]cholecalciferol, metabolite E was predominantly formed. Metabolite D was predominantly formed from cholecalciferol. Metabolites D and E differ from any known cholecalciferol metabolites. 3. The intestine was found to be the tissue capable of carrying out the transformation of 25-hydroxycholecalciferol into metabolite E. 4. 25-Hydroxycholecalciferol and metabolite E were localized in the digestive gland of the snail, the tissue responsible for the absorption of Ca2+ and its storage. Metabolite D was not localized in any specific tissue.

Animals↗
PubMed1979

Response of neonatal hypocalcaemia to 1 alpha-hydroxyvitamin D3.

Administration of 1 alpha-OH-D3 to hypocalcaemic neonates (mean +/- SD, serum calcium 1.50 +/- 0.13 mmol/l) significantly increased serum calcium in all 24 infants within 48 hours after starting therapy (mean +/- SD 1.83 +/- 0.23 mmol/1). The time required to correct hypocalcaemia was significantly shorter (2.04 +/- 0.56 days) in infants treated with 1 alpha-OH-D3, than in 24 infants treated with calcium gluconate infusions (4.12 +/- 1.0 days). Treatment with 1 alpha-OH-D3 was effective, easy to maintain, and produced no side effects.

Calcium Gluconate↗
PubMed1978

Synthesis of 1 alpha-hydroxy[7-3H]cholecalciferol and its metabolism in the chick.

1. 1 alpha-Hydroxy[7-3H]cholecalciferol (specific radioactivity of 2-Ci/mmol) was synthesized, and its metabolism in chicks studied. 2. 1 alpha-Hydroxy[7-3H]cholecalciferol was metabolized very rapidly in the chick to 1 alpha,25-dihydroxy[7-3H]cholecalciferol and to a metabolite less polar than 1 alpha-hydroxycholecalciferol. Intestine exhibited highest accumulation of 1 alpha-25-dihydroxy[7-3H]cholecalciferol, and liver exhibited highest accumulation of the non-polar metabolite. 3. Tissue uptake of 1 alpha-hydroxy[7-3H]cholecalciferol and its metabolites in chicks that were dosed continuously for 16 days with 1 alpha-hydroxy[7-3H]cholecalciferol did not exceed by very much that observed in tissues obtained from chicks that were dosed with a single injection of 1 alpha-hydroxy[7-3H]cholecalciferol 24 h before killing, except for liver and kidney. 4. Lowest accumulation of metabolites was noted in muscle and bone, and for the latter, highest uptake of 1 alpha,25-dihydroxy[7-3H]cholecalciferol was noted in the epiphysial periosteum and the metaphysis. 5. Formation of 1 alpha,24,25-trihydroxy[7-3H]cholecalciferol was not observed in the chicks that were dosed continuously with 1 alpha-hydroxy[7-3H]cholecalciferol, despite the fact that plasma calcium and phosphorus were normal and despite the presence of renal 24-hydroxylase activity. 6. The vitamin D status of the chicks did not appear to affect the metabolic profile of the administered 1 alpha-hydroxy[7-3H]cholecalciferol.

Animals↗
PubMed1978

The parotid gland: a new target organ for vitamin D action.

Radioactively labelled cholecalciferol was administered continuously to rats which were fed a vitamin D-deficient diet. It has been possible to show that all the metabolites of the cholecalciferol which normally occur in known target tissues of vitamin D are present in the parotid gland, and the pattern resembled that obtained for the kidney, a known target tissue for vitamin D action. The accumulation of cholecalciferol metabolites in the parotid gland was shown to be functional, as a calcium-binding protein was found to be present in the gland, possessing similar properties to the renal vitamin D-dependent calcium-binding protein.

Animals↗
PubMed1978

Vitamin D metabolism and expression in rats fed on low-calcium and low-phosphorus diets.

1. Cholecalciferol, radioactively labelled with both (14)C and (3)H, was administered weekly for 7 weeks to rats that had been depleted of vitamin D for 4 weeks before repletion with the radioactive vitamin. This permitted measurement of the steady-state effect on vitamin D metabolism of low-calcium and low-phosphorus regimens, as compared with a normal mineral intake. These dietary manoeuvres were carried out during the last 3 weeks of repletion. Cholecalciferol, 25-hydroxycholecalciferol and 1,25-dihydroxycholecalciferol were determined in plasma, intestine, kidney and bone. Ca(2+)-binding-protein content was measured in intestine and kidneys of comparable animals. 2. In rats on the low-calcium diets, 1,25-dihydroxycholecalciferol concentration was elevated in plasma, bone, kidney and intestine, and intestinal Ca(2+)-binding protein was increased to over twice the concentration found in the control animals. 3. The low-phosphorus regimens led to a decrease in plasma phosphate and 1,25-dihydroxycholecalciferol in all tissues studied, for the latter to the point where it was undetectable in plasma and bone. Intestinal and renal concentrations of Ca(2+)-binding protein were unchanged in the low-phosphate-intake group and decreased in the very-low-phosphate-intake group. 4. It is concluded that in the rat, unlike in the chick, hypophosphataemia is not associated with a stimulation of the production of 1,25-dihydroxycholecalciferol or its expression in the synthesis of Ca(2+)-binding protein. Therefore the plasma phosphate concentration does not appear to be directly involved in the regulation of the functional metabolism of vitamin D.

Animals↗