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PubMed1985

[Vitamin D sterol in human milk, cow's milk and baby food].

A review is given of the results of vitamin D determinations in human and cow's milk using physico-chemical methods. Thereby only parent vitamin D is determined. Further, the results obtained with protein-binding assays are discussed in detail. With the aid of these newer methods the concentrations of hydroxylated vitamin D derivatives can also be measured. A comparison of the concentration of these vitamin D metabolites in human milk and infant formulas based upon cow's milk suggests that the higher anti-rachitic activity of human milk is connected with its higher concentration of 25-hydroxy-vitamin D.

Animals↗
PubMed1984

Effects of weight loss on serum 1,25-(OH)2-vitamin D concentrations in adults: a preliminary report.

During a review of 42 metabolic studies in healthy women and men we observed that serum 1,25-(OH)2-D concentrations were directly correlated to the observed daily changes in body weight (r = 0.68; P less than 0.001) and to caloric intake/kg/day (r = 0.39; P = 0.01). These relationships could not be accounted for by related and physiologically expected changes in serum Ca or iPTH concentrations. However, serum 1,25-(OH)2-D concentrations were observed to be inversely correlated to serum PO4 levels (r = -0.44; P = 0.004). In addition, serum PO4 levels were inversely correlated to the daily changes in body weight (r = -0.40; P = 0.009). Since dietary sodium intake averaged 142 mmol/day, it is unlikely that the observed changes in weight were the result of changes in salt and water balance. Thus it seems reasonable to speculate that serum 1,25-(OH)2-D concentrations may vary directly with energy balance, as reflected by changes in body weight. This effect may be mediated by alterations in PO4 metabolism. The accurate assessment of serum 1,25-(OH)2-D levels thus appears to require several measurements over time periods during which body weight is stable.

Adult↗
PubMed1984

Evidence for abnormal regulation of circulating 1 alpha, 25-dihydroxyvitamin D in patients with pulmonary tuberculosis and normal calcium metabolism.

Available evidence indicates that hypercalcemia in pulmonary tuberculosis results from increases in circulating 1 alpha, 25-dihydroxyvitamin D [1 alpha, 25(OH)2D]. To further characterize vitamin D metabolism in this disorder, the effects of vitamin D, 100,000 units a day for 4 days, were compared in 25 normal subjects and 11 patients with active pulmonary tuberculosis who were normocalcemic and had not had hypercalcemia. Serum calcium, phosphorus, 25-hydroxyvitamin D (25-OHD) and 1 alpha, 25(OH)2D were measured. Whereas vitamin D increased mean serum 25-OHD from 20 +/- 2 (+/- SE) to 40 +/- 5 ng/ml (P less than 0.001) and did not change mean serum 1 alpha, 25(OH)2D in the normals (33 +/- 2 vs. 31 +/- 2 pg/ml), it increased mean serum 25-OHD from 21 +/- 4 to 55 +/- 13 ng/ml (P less than 0.05) and mean serum 1 alpha, 25(OH)2D from 28 +/- 2 to 35 +/- 3 pg/ml (P less than 0.05) in the patients. Serum calcium was normal and remained within the normal range in all subjects and patients. The findings indicate that there is a modest but significant abnormality in the regulation of circulating 1 alpha, 25(OH)2D in normocalcemic patients with pulmonary tuberculosis. The results are similar to those previously reported by us in normocalcemic patients with sarcoidosis.

Adult↗
PubMed1981

Protective effect on vitamin D2 on bone apposition from the inhibitory action of hydrocortisone in rats.

Using the technique of short interval sequential tetracycline labeling, it was documented that the apposition of mineralized bone matrix in adult male Sprague-Dawley rats was inhibited by hydrocortisone. The inhibition occurred as early as six days after the onset of the treatment and was dose dependent over a dose range of 0.62 to 20 mg per kg body weight per day. Vitamin D2 supplements by injection protected bone from this hydrocortisone action. 64 I. U. of vitamin D2 injected daily was able to prevent the inhibition of bone apposition by 20 mg per kg body weight per day of hydrocortisone. The results imply that vitamin D or its metabolites may compete with hydrocortisone in some cellular mechanisms and support the usefulness of vitamin D supplements in the treatment and the prevention of steroid-induced osteoporosis.

Animals↗
PubMed1981

Serum 1,25-dihydroxyvitamin D concentration in hypophosphatemic vitamin D-resistant rickets.

Fasting serum 1 alpha, 25-dihydroxyvitamin D [1,25-(OH)2D] levels were measured in 3 groups of hypophosphatemic vitamin D-resistant rickets (VDRR) patients; those untreated; those treated with vitamin D and phosphate; and those treated with 1,25-(OH)2D3 and phosphate. In the untreated patients, the mean 1,25-(OH)2D level was higher than in our age-matched control group. Except for one at 66 pg/ml, individual values were however within normal limits. Long term vitamin D2 therapy was accompanied by a slight but significant decrease in 1,25-(OH)2D concentrations; nonetheless the levels remained within the normal range. In the third group of patients, the concentration of 1,25-(OH)2D rose to supranormal levels when sampling was done 1-3 hours after administration of the hormone, decreasing rapidly to levels below that of normal subjects when the specimens were collected 12-24 hours later. Our data show that an alteration of the vitamin D activation pathway is unlikely to be part of the pathogenic mechanism underlying the VDRR condition.

Adolescent↗
PubMed1981

Serum levels of 25-hydroxyvitamin D in postmenopausal osteoporosis.

Serum concentrations of 25-hydroxy-vitamin D were measured in a group of women with symptomatic postmenopausal osteoporosis, assessed by bone biopsy. A competitive protein binding assay was used, which included a chromatographic step. Accurate surveys of dietary or therapeutic vitamin D intake and light environment were obtained in each patient. Women with severe postmenopausal osteoporosis were found to have significantly (P less than 0.001) higher serum levels of 25-hydroxyvitamin D than age-matched normal women, the mean values being 27.5 ng/ml (+/- 13.6 SD) and 9.2 ng/ml (+/-5.7), respectively. The authors hypothesize that the reduction in 1,25-dihydroxyvitamin D, recently reported in postmenopausal osteoporotic women, might be responsible for the increased serum levels of 25-hydroxyvitamin D through an inadequate product inhibition of liver vitamin D 25-hydroxylase.

25-Hydroxyvitamin D 2↗
PubMed1982

Serum calcium regulating hormones in the perinatal period.

To clarify perinatal vitamin D metabolism, we measured 25-hydroxyvitamin D (25OHD), 24,25-dihydroxyvitamin D [24,25(OH)2D], 1,25-dihydroxyvitamin D [1,25(OH)2D], calcium (Ca), phosphorus (P), parathyroid hormone (PTH), and human calcitonin (CT) in paired maternal, cord, and infant serum. Cord serum 25OHD was significantly lower than the maternal level, and cord serum 24,25(OH)2D was also significantly below the maternal concentrations. Maternal, cord, and infant serum 1,25(OH)2D, on the other hand, was significantly higher than the normal adult level. The serum PTH was low, but the CT concentration was high in the cord. Cord serum Ca and P levels were significantly higher than maternal. The reason for the elevated circulating 1,25(OH)2D level in the perinatal period is uncertain, and we speculate that the possible factors are gonadal steroids, placental lactogen, prolactin, and CT. In addition, serum 24,25(OH)2D and 1,25(OH)2D concentrations are under some control by the fetus.

Adult↗
PubMed1982

Effect of the administration of 1,25-dihydroxyvitamin D3 on serum levels of 25-hydroxyvitamin D in postmenopausal osteoporosis.

Serum concentrations of 25-hydroxyvitamin D were measured in a group of women with symptomatic postmenopausal osteoporosis, before and after long-term treatment with physiological doses of 1,25-dihydroxyvitamin D3. A competitive protein binding assay was used, which included a chromatographic step. The treatment resulted in a significant decrease in serum 25-hydroxyvitamin D levels that were higher than normal in basal conditions, the mean values before and after therapy being 27.7 ng/ml (+/- 17.1 SD) and 19.7 ng/ml (+/- 12.7), respectively. These findings seem to confirm the hypothesis that an inadequate product-inhibition of liver 25-hydroxylase is responsible for the increased basal levels of 25-hydroxyvitamin D found in postmenopausal osteoporosis.

25-Hydroxyvitamin D 2↗