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Biomedical subjects

H F DeLuca

Publications and source records attributed to H F DeLuca.

At least 469 records · Page 26Linked to original sources
PubMed1979

Vitamin D metabolism during pregnancy and lactation in the rat.

The plasma concentration of the major vitamin D metabolites; 25-hydroxyvitamin D, 1,25-dihydroxyvitamin D, and 24,25-dihydroxyvitamin D were measured during pregnancy and lactation in the adult female rat. The concentrations of these metabolites were also measured in rat pups during lactation and after weaning. The plasma concentration of 1,25-dihydroxyvitamin D in the adult female increases from a control value of 26 pg/ml to 86 pg/ml during the latter stages of pregnancy, reaches a peak of 158 pg/ml during lactation, and then returns to control levels by 3 weeks postweaning. Plasma concentrations of 24,25-dihydroxyvitamin D fall dramatically during pregnancy from a control level of 3.9 ng/ml to 1.6 ng/ml remain low during lactation, and return to control levels by 3 weeks postweaning. In the neonatal rat pup at 14 days postpartum, 1,25-dihydroxyvitamin D plasma concentration is 25 pg/ml and 24,25-dihydroxyvitamin D concentration is 2.8 ng/ml. By day 25 postpartum, 1,25-dihydroxyvitamin D concentrations reached levels of 101 pg/ml, whereas 24,25-dihydroxyvitamin D concentrations fell to 1.9 ng/ml.

Age Factors↗
PubMed1979

On the physiological basis of vitamin A-stimulated growth.

The influence of vitamin A depletion on tissue composition was studied in rats that were marginally vitamin A deficient, i.e. at their weight plateau stage. The total number of cells (DNA) was decreased in most organs as a result of vitamin A depletion. In thymus, spleen and the sublingual glands there was also a dramatic reduction in the number of cells per gram of tissue and in thymus and sublingual glands there was an increase in the protein to DNA ratio as a result of absence of dietary.vitamin A. We present the hypothesis that vitamin A stimulates growth by a direct role in cell replication in addition to or instead of stimulating the differentiation of epithelial and bone cells.

Animals↗
PubMed1979

Evidence that increased circulating 1 alpha, 25-dihydroxyvitamin D is the probable cause for abnormal calcium metabolism in sarcoidosis.

Mean plasma 1(alpha),25-dihydroxyvitamin D[1(alpha),25(OH)(2)D] was significantly increased and serum parathyroid hormone was suppressed in three patients with sarcoidosis and hypercalcemia. Prednisone lowered the mean plasma 1(alpha),25(OH)(2)D to normal range and corrected the hypercalcemia. To elucidate the mechanism for the increased sensitivity to vitamin D in this disorder, the effects of orally-administered vitamin D(2) were determined in seven normal subjects, four patients with sarcoidosis and normal calcium metabolism and three patients with sarcoidosis and a history of hypercalcemia who were normocalcemic when studied. Serum and urinary calcium, serum 25-hydroxyvitamin D (25-OHD), plasma 1(alpha),25(OH)(2)D and, in some studies, calcium balance were measured. Vitamin D(2), 250 mug a day for 12 d, produced little, if any, change in mean plasma 1(alpha),25(OH)(2)D and in urinary calcium in the normals and in the patients with normal calcium metabolism. In contrast, vitamin D(2) produced increases in plasma 1(alpha),25(OH)(2)D from concentrations which were within the normal range (20-55 pg/ml) to abnormal values and increased urinary calcium in two patients with abnormal calcium metabolism. In an abbreviated study in the third patient, vitamin D(2), 250 mug a day for 4 d, also increased plasma 1(alpha),25(OH)(2)D abnormally from a normal value. There was a highly significant correlation between plasma 1(alpha),25(OH)(2)D and urinary calcium. Serum 25-OHD and serum calcium remained within the normal range in all subjects and patients. These findings provide evidence that the defect in calcium metabolism in sarcoidosis probably results from impaired regulation of the production and(or) degradation of 1(alpha),25(OH)(2)D. Prednisone may act to correct the abnormal calcium metabolism by reducing circulating 1(alpha),25(OH)(2)D.

Adult↗
PubMed1979

Intestinal calcium absorption and serum vitamin D metabolites in normal subjects and osteoporotic patients: effect of age and dietary calcium.

Intestinal calcium absorption assessed by a double-isotope method, decreased significantly with aging in 94 normal subjects (r = -0.22, P < 0.025). In 52 untreated patients with postmenopausal osteoporosis, calcium absorption was significantly lower than normal when either age or habitual calcium intake was used as a covariable (P < 0.001). Serum 25-hydroxyvitamin D (25-OH-D) and 1,25-dihydroxyvitamin D (1,25(OH)(2)D) were measured in 44 normal subjects and 27 osteoporotic patients. For all normals, calcium absorption and serum 1,25(OH)(2)D were positively correlated (r = 0.50, P < 0.001). In nonelderly normal subjects (ages 30-65 yr), dietary calcium intake correlated inversely with both calcium absorption (r = -0.39, P < 0.01) and with serum 1,25(OH)(2)D (r = -0.50, P < 0.01). Both osteoporotic patients and elderly normal subjects (ages 65-90 yr) differed from nonelderly normals in that these correlations were not present. In addition although serum 25-OH-D was normal, serum 1,25(OH)(2)D was significantly decreased in both osteoporotic patients and elderly normals (P < 0.001). In osteoporotic patients, calcium absorption increased significantly (P < 0.001) after 7 d administration of a small dose (0.4 mug/d) of synthetic 1,25(OH)(2)D(3). In osteoporotics mean serum immunoreactive parathyroid hormone was either normal (COOH-terminal assay) or low (NH(2)-terminal assay) relative to age-matched controls, and mean serum phosphate was increased. The data suggest that inadequate metabolism of 25-OH-D to 1,25(OH)(2)D contributes significantly to decreased calcium absorption and adaptation in both osteoporotics and elderly normal subjects. In patients with osteoporosis this abnormality could result from a decrease in factors that normally stimulate 1,25(OH)(2)D production, such as the decreased parathyroid hormone secretion and increased serum phosphate demonstrated in this group. In elderly subjects a primary abnormality in metabolism of 25-OH-D to 1,25(OH)(2)D, analagous to that seen in aging rats, cannot be excluded.

Adult↗
PubMed1979

Production of 1,25-dihydroxyvitamin D3 and formation of medullary bone in the egg-laying hen.

Renal 25-hydroxyvitamin D-1-hydroxylase, the percentage of medullary bone in the femur, plasma calcium, and plasma phosphorus were measured in female chickens reaching maturity. These parameters and plasma 1,25-dihydroxyvitamin D levels were also measured during the daily egg-laying cycle in mature hens. The renal 25-hydroxyvitamin D3-l-hydroxylase becomes elevated in maturing hens before and at the time of ovulation. This elevation in the 1-hydroxylase correlates with the elevation in total plasma calcium concentration but lags and at the time of ovulation and is followed by a further elevation of plasma 1,25-dihydroxyvitamin D levels. The plasma 1,25-dihydroxyvitamin D level remains high until 12 h postovulation. At this time, it falls to the preovulation level. No relationship could be found between the plasma 1,25-dihydroxyvitamin D levels and the changes in medullary bone found during the egg-laying cycle. However, plasma 1,25-dihydroxyvitamin D levels are highest immediately before and during the egg shell calcification phase of the egg-laying cycle.

25-Hydroxyvitamin D3 1-alpha-Hydroxylase↗
PubMed1979

Potential use of 1,25-dihydroxycholecalciferol for prevention of parturient paresis.

Twelve cows, at least third parity, were assigned randomly to either a control or treatment group. Treated cows received .4 mg of the vitamin D metabolite, 1,25-dihydroxycholecalciferol intramusculary in 5 ml corn oil. Intramuscular injections were started 5 days before predicted calving with reinjections every 5 days until calving. Incidence of parturient paresis was 0 and 33% (2 of 6) in the treated and control groups. Response to treatment was rapid with elevated calcium in serum approximately 12 h postinjection. Treatment maintained or elevated calcium and phosphorus concentrations in serum during the critical period, 24 h pre- to 48 h postpartum, when milk fever is most likely to occur. There was, however, no significant difference between treatments at 72 h postpartum. Based on these observations 1,25-dihydroxycholecalciferol holds promise as a preventative of parturient paresis; however, further studies are needed on application and safety.

Animals↗
PubMed1978

Reduction of serum-1, 25-dihydroxyvitamin-D3 in children receiving glucocorticoids.

Serum-1,25-dihydroxyvitamin-D3 (1,25-[OH]2D3) was subnormal in children receiving long-term glucocorticoid treatment for various glomerular diseases, including nephrotic syndrome. In children with chronic glomerulonephritis not treated with glucocorticoids who had similar serum-creatinine with glucocorticoids who had similar serum-creatinine concentrations, serum-1,25-dihydroxyvitamin-D3 concentrations resembled those in healthy controls, indicating that glomerular renal disease per se does not account for reduced serum-1,25(OH)2DE concentrations in steroid-treated patients. The reduction in concentration of this most active vitamin-D metabolite correlated with the dose of steroid administered and with reduction in forearm bone mineral content measured by the photon absorption technique. Reduced serum-1,25-(OH)2D3 concentration may be important in the pathogenesis of steroid-induced osteopenia.

Administration, Oral↗
PubMed1978

Serum 1,25-dihydroxyvitamin D levels in normal subjects and in patients with hereditary rickets or bone disease.

The serum concentration of 1,25-dihydroxylvitamin D (1,25-[OH]2D) in normal children and in children with inherited diseases of bone was compared by use of a competitive binding assay. Observed values were: in 12 normal children and adolescents, 37.1 +/- 1.9 pg per milliliter (mean +/- S.D.); in 14 patients with X-linked hypophosphatemic rickets treated with vitamin D2 and phosphate supplements, 15.6 +/- 7.8 (P less than 0.01 versus control); in six patients with autosomal recessive vitamin D dependency treated with vitamin D2, 9.5 +/- 2.9 (P less than 0.01 versus control); and in four untreated patients with autosomal dominant hypophosphatemic (non-rachitic) bone disease, 30.2 +/- 6.3 (not significantly different from the controls). The difference in bone disease between X-linked hypophosphatemia (severe) and hypophosphatemic bone disease (mild) at comparable low serum levels of phosphate implies that 1,25-(OH)2D and phosphate may have independent roles in the pathogenesis of defective bone mineralization.

Adolescent↗
PubMed1978

Incorportion of oxygen-18 into the 25-position of cholecalciferol by hepatic cholecalciferol 25-hydroxylase.

The oxygen enzymically inserted as a hydroxy function by rat liver post-mitochondrial fraction into the 25-position of cholecalciferol to giver 25-hydroxycholecaliferol is derived exclusively from molecular O2. Therefore like the other two cholecalciferol hydroxylases, i.e. 25-hydroxycholecalciferol 1alpha-hydroxylase and 25-hydroxycholecalciferol 24-hydroxylase, the cholecalciferol 25-hydroxylase is also a mono-oxygenase ('mixed-function oxidase').

Animals↗
PubMed1978

Isolation and identification of 5, 6-epoxyretinoic acid: a biologically active metabolite of retinoic acid.

A highly biologically active metabolite of retinoic acid (8III) has been isolated in pure form from intestinal mucosa of vitamin A deficient rats given [3H]retinoic acid. This metabolite has been positively identified as 5, 6-epoxyretinoic acid based on the ultraviolet absorption spectrum and mass spectrum of its methylated derivative. This identification was confirmed by cochromatography of the methylated metabolite and synthetic methyl 5, 6-epoxyretinoate on reverse-phase and straight-phase high-pressure liquid chromatography. The 5, 6-epoxyretinoic acid is a true in vivo generated metabolite of retinoic acid and not an artifact of the isolation procedure. In addition, 5, 8-oxyretinoic acid previously isolated in this laboratory from intestinal mucosa was probably generated from 5, 6-epoxyretinoic acid by the acidic conditions used in the extraction and isolation of the 5, 8-oxyretinoic acid.

Animals↗
PubMed1978

Response of 1alpha,25-dihydroxyvitamin D3 to hypocalcemia in human subjects.

We determined the response of 1alpha,25-dihydroxyvitamin D3 after mithramycin-induced hypocalcemia in eight subjects with polyostotic Paget's disease of bone. Thirty-six hours after infusion of mithramycin (25 microgram per kilogram), the average calcium declined from 9.9 +/- 0.14 (S.E.M.) to 8.0 +/- 0.19 mg per deciliter (P less than 0.005). Serum parathyroid hormone increased from 122 +/- 6 to 226 +/- 36 microliter eq per milliliter (P less than 0.05), serum phosphate decreased from 3.8 +/- 0.11 to 2.9 +/- 0.14 mg per deciliter (P less than 0.005), and urinary cyclic 3,5'-adenosine monophosphate increased from 4.6 +/- 0.35 to 7.5 +/- 0.80 mumol per gram of creatinine (P less than 0.005). Serum 1alpha25-dihydroxyvitamin D3 rose from 98 +/- 12 to 332 +/- 61 pM (P less than 0.05), the increase following the changes in parathyroid hormone and phosphate by 12 to 24 hours. When this lag period was taken into account, there was a significant relation (P less than 0.01) between the increase in 1alpha,25-dihydroxyvitamin D3 and changes in parathyroid hormone (correlation coefficient, r = +0.91) and phosphate (r = -0.96). The relatively rapid response of 1alpha,25-dihydroxyvitamin D3 to hypocalcemia occurs with a time course consistent with regulation by parathyroid hormone and phosphate.

Aged↗