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PubMed1981

Relative effectiveness of vitamin D metabolites in increasing bone mineral solubility.

Weanling rats were given a vitamin D-deficient diet containing 1.4% calcium and 1.0% phosphorus. After 4 weeks these deficient animals were injected for 7 days with selected doses of one of the following vitamin D metabolites: 25(OH)D3, 1,25(OH)2D3, 24,25(OH)2D3, 25,26(OH)2D3 or the ethanol vehicle. A vitamin D-replete group was placed on the same diet but injected with 50 IU of vitamin D3 once a week for the entire 5-week period. By the use of a modified Ussing chamber [1], the measurements of calcium fluxes into and from the rat calvaria were possible. These data enabled the apparent mineral solubilities to be derived. After 5 weeks on this diet the vitamin D-deficient rats had low levels of serum calcium (1.41 mM) and decreased mineral solubility when compared to the vitamin D-replete group. The apparent solubility of the bone mineral increased toward the vitamin D-replete level in calvaria from vitamin D metabolite-treated rats. However, these changes did not directly reflect the alterations in the level of serum calcium. At any given dose level, 1,25(OH)2D3 was the most effective metabolite in increasing serum calcium. In fact, the high dose (250 pmoles/day) was hypercalcemic. Next in effectiveness was 25(OH)D3. These two metabolites were equally effective in increasing mineral solubility. At a 10 times higher dose, the 24,25(OH)2D3 metabolite was able to normalize serum calcium and improve but not normalize mineral solubility. At the high dose (260 pmoles/day), the 25,26(OH)2D3 metabolite caused no effect on mineral solubility and minimal increases in serum calcium.

Animals↗
PubMed1981

Action of vitamin D metabolites on PTH secretion in man.

We have examined the effects of metabolites of vitamin D [25OHD3, 1,25(OH)2D3, 24,25(OH)2D3, and 25,26(OH)2D3] on serum calcium and iPTH in human deficient-D osteomalacia. The four metabolites decreased iPTH, but only for 1,25(OH)2D3 was a significant correlation between increase of serum calcium and decrease of iPTH observed. The 24,25(OH)2D3 and 25,26(OH)2D3 decreased iPTH despite a decrease of serum calcium at the beginning of treatment. The 25OHD decreased iPTH before increased serum calcium. These results could be interpreted as a direct effect of metabolites of vitamin D on PTH secretion. However, the conversion of other metabolites and the calcium concentration in parathyroid cells must be determined before this hypothesis can be accepted.

24,25-Dihydroxyvitamin D 3↗
PubMed1981

Decreased 1,25-dihydroxycholecalciferol and increased 25-hydroxy- and 24,25-dihydroxycholecalciferol in tissues of rats treated with thyroxine.

The effect of thyroxine on the metabolism of vitamin D was investigated in rats. Vitamin D depleted rats were repleted by injections of radiolabelled cholecalciferol or 25-hydroxycholecalciferol (25OHD3). After 3 weeks, a state of hyperthyroidism was induced by daily injections of L-thyroxine for 21 days. The lipid extracts of the Plasma and tissues were analyzed by successive Sephadex LH-20 and high pressure liquid chromatography. The concentrations of 25OHD3 and of 24,25-dihydroxycholecalciferol (24,25 (OH)2D3) were significantly higher and those of cholecalciferol and of 1,25-dihydroxycholecalciferol (1,25(OH)2D3) were significantly lower in the plasma and tissues of animals treated with thyroxine than in controls. The present study suggests that alterations in the metabolism of vitamin D may be involved in the disturbances of calcium metabolism observed in hyperthyroidism.

24,25-Dihydroxyvitamin D 3↗
PubMed1981

Increased 1,25-dihydroxyvitamin D3 synthesis in rats fed a high-phosphorus diet.

Rats fed vitamin D-deficient diets containing 0.6% Ca and 0.3%, 0.6%, 1.2%, or 1.8% P exhibited progressive increments of hypocalcemia and hyperphosphatemia. In vitro assay of 25-hydroxyvitamin D3-1-alpha-hydroxylase (1-alpha-hydroxylase) activity in isolated kidney cortical mitochondria showed that hyperphosphatemia in the presence of hypocalcemia was associated with an increase in enzyme activity. The results indicate that the stimulation of 1-alpha-hydroxylase associated with depressed plasma Ca in rats fed a high-P diet overrides any inhibition of the enzyme that may be caused by excess plasma phosphate.

25-Hydroxyvitamin D3 1-alpha-Hydroxylase↗
PubMed1982

Biochemical findings in blood of aged patients with femoral neck fractures: a contribution to the detection of occult osteomalacia.

A study was made in Geneva of 44 patients with femoral neck fractures and no risk factor of osteomalacia to determine concentrations of 25OHD3, calcium, phosphorus, alkaline phosphatase, albumin, and globulins in blood. The results were compared with those obtained for control groups of adult and aged subjects, as well as of 21 subjects operated on for hip osteoarthritis. For the detection of occult osteomalacia, femoral head bone tissue from 14 patients with fractures was examined by histomorphometric methods. In more than a third of the cases, 25OHD3 and serum albumin values were lower than those found for adult and even aged control subjects. Some slight histological signs of osteomalacia were observed in 1 patient with a femoral neck fracture, but there was no correlation between the histologic and the blood data. In practice, when dealing with aged people with no obvious risk of osteomalacia, it is important that a systematic antiosteomalacia treatment consisting of large supplements of vitamin D be avoided and that the conditions of diet and living be carefully controlled.

Adult↗
PubMed1982

Serum calcitonin concentrations in premature infants during the first 12 weeks of life.

Twenty-eight premature infants of mean gestation 30.9 +/- 2.5 weeks and mean birth weight 1175 +/- 206 g had repeated serum calcitonin concentrations determined over the first 12 weeks of life. Serum calcitonin concentrations slowly fell but remained elevated even at 12 weeks of age [normal adult = 71 +/- 48, 1 week (N = 15) = 327 +/- 167, 3 week (N = 23) = 270 +/- 129, 6 week (N = 16) = 249 +/- 154, 9 week (N = 13) = 214 +/- 108, 12 week (N = 12) = 174 +/- 11]. Throughout this period, serum total calcium was normal or low (8.4 +/- .8-9.3 +/- 1.0). Serum phosphorus was normal or low (6.0 +/- 1.4-6.5 +/- 1.0), and serum magnesium was normal (1.7 +/- 0.24-1.8 +/- 0.34). The reason for the sustained elevation of serum calcitonin in these very small, sick, premature infants in unclear.

Alkaline Phosphatase↗
PubMed1982

Etiology of hypercalcemia in a patient with Addison's disease.

A case is reported of a hypercalcemic patient with primary Addison's disease. A combination of increased calcium input into the extracellular space and reduced calcium removal by the kidney accounted for the hypercalcemia. The mechanisms responsible for the reduction in calcium removal were decreased glomerular filtration and increased tubular calcium reabsorption. Both renal factors were secondary to volume depletion and improved rapidly during rehydration with saline infusion. The enhanced calcium mobilization was probably of skeletal origin. It persisted irrespective of volume status until hydrocortisone treatment was instituted. Serum 1,25-dihydroxyvitamin D3 levels were below 10 pg/ml, even after normalization of the glomerular filtration rate, but returned slowly to the normal range during corticosteroid substitution. Serum 25-hydroxyvitamin D3 and parathyroid hormone levels were within the normal range. Our case report therefore demonstrates that physiological amounts of glucocorticoids reduce bone resorption, normalize serum calcium, and restore the production of 1,25-dihydroxyvitamin D3.

Addison Disease↗
PubMed1986

Pancreatic secretion in man with subclinical vitamin D deficiency.

The effects of subclinical vitamin D deficiency and vitamin D supplementation on oral glucose tolerance and secretion of pancreatic hormones were studied in 10 diphenylhydantoin-treated epileptic patients and 15 geriatric patients. Their mean serum concentrations of 25-hydroxyvitamin D3 and 1,25-dihydroxyvitamin D3 decreased markedly, but returned to normal within 2 weeks of oral supplementation with 25-hydroxyvitamin D3. The serum concentration of ionized calcium was within the normal range before treatment, and remained unchanged. Serum parathyroid hormone was increased during vitamin D deficiency, but decreased significantly (p less than 0.05) afterwards. In vitamin D-deficient epileptic and geriatric patients, the 2- and 3-h insulin levels after glucose ingestion were increased when compared with control values, and glucagon secretion was not suppressed by glucose. Oral glucose tolerance of both groups of patients did not change after 25-hydroxyvitamin D3 supplementation. Insulin secretion remained unchanged in geriatric patients, but was reduced to normal values in epileptic patients. Glucagon suppressibility by glucose was partly restored after vitamin D supplementation in epileptic patients but not in geriatric patients. In contrast to that observed in severely vitamin D-deficient rats or rabbits, correction of subclinical vitamin D deficiency failed to enhance insulin secretion or to improve glucose tolerance in man.

Age Factors↗
PubMed1986

Bone disorder following partial and total gastrectomy with reference to bone mineral content.

To study post-gastrectomy metabolic bone disorders, we measured the radial bone mineral content (BMC), serum levels of calcium, inorganic phosphorus, alkaline phosphatase, and 25-hydroxyvitamin D(25-OH-D) in 59 patients with partial- and 39 patients with total gastrectomy. Total gastrectomy patients manifested a higher incidence of decreased BMC levels than did partial gastrectomy patients (56 per cent vs. 25 per cent). Patients subjected to the Billroth II procedure, especially females, manifested abnormally low BMC values. The decline in BMC was age-related; it was pronounced in females. At 10 years postoperatively, many of the partial gastrectomy patients manifested markedly low BMC levels; in totally gastrectomized patients this finding was made at less than 5 years postoperatively. Approximately 30 per cent of our patients showed abnormalities in serum minerals, alkaline phosphatase or 25-OH-D.

Alkaline Phosphatase↗
PubMed1988

Suppression of rat hepatic vitamin D-25-hydroxylase by cholecalciferol, but not by 25-hydroxy- or 1,25-dihydroxymetabolites.

Hepatic vitamin D-25-hydroxylase activity is greater in vitamin D-depleted than replete animals. We investigated whether vitamin D itself or a metabolite of vitamin D was responsible for modulating the activity of vitamin D-25-hydroxylase. Accordingly, we repleted vitamin D-depleted rats with subcutaneous injections of 2600, 520, and 130 pmoles of cholecalciferol (D3), 25-hydroxycholecalciferol (25(OH)D3), and 1,25-dihydroxycholecalciferol (1,25(OH)2D3), respectively, for up to 3 weeks. Repletion resulted in accelerated weight gain and in increased activity of gut mucosal alkaline phosphatase. Using an improved assay to measure vitamin D-25-hydroxylase activity in liver homogenates, we found 78% reduction (P less than 0.001) in the D3-repleted group, maximal by 1 week, in contrast to no change in those groups treated with D3 metabolites. D3, 25(OH)D3, and D3-esters remaining in livers at the time of assay were estimated in a parallel experiment using [3H]D3-repleted rats. Residual D3 accounted for only a 9% dilution of substrate in the assay. 25(OH)D3 was present in the liver at concentrations two orders of magnitude lower than the amount required to inhibit vitamin D-25-hydroxylase activity in vitro. D3 esters had no inhibitory effect in vitro at 250-fold excess of that found in the repleted rat liver. Vitamin D appears to modulate its D-25-hydroxylase activity in biological systems by a mechanism other than feedback inhibition by 25(OH)D3, 1,25(OH)2D3, or D3-esters.

Animals↗
PubMed1986

Does 24R,25(OH)2-vitamin D3 prevent postmenopausal bone loss?

The effect of oral 24R,25(OH)2-vitamin D3 as a prophylactic for postmenopausal bone loss was examined. Fifty-eight healthy, early postmenopausal women entered a double blind therapeutic trial for 2 years. After an initial examination the women were randomized to treatment with 10 micrograms 24R,25(OH)2D3 daily or placebo. Participants were thereafter examined every 3 months (nine examinations in all). In both groups the forearm bone mineral (measured by single photon absorptiometry), the lumbar spine mineral, and the total body mineral (measured by dual photon absorptiometry) fell significantly and at the same magnitude. Furthermore, serum calcium, serum alkaline phosphatase concentration, and fasting urinary hydroxyproline were unchanged, as were the 24-hour urinary calcium excretion and the intestinal radiocalcium absorption. Our findings demonstrate that 24R,25(OH)2D3 treatment has no prophylactic effect on postmenopausal bone loss and does not alter calcium metabolic variables.

24,25-Dihydroxyvitamin D 3↗
PubMed1986

The effect of endogenous estrogen fluctuation on metabolism of 25-hydroxyvitamin D.

To test the hypothesis that estrogen modulates the metabolism of 25-hydroxyvitamin D (25(OH)D) to 1,25-dihydroxyvitamin D (1,25(OH)2D) and 24,25-dihydroxyvitamin D (24,25(OH)2D), we studied 20 normal premenopausal women at four consecutive weekly intervals during one menstrual cycle. Estrogen stimulation was semiquantitatively defined into baseline, low-grade, or medium-grade categories, based on endogenous estrone and estradiol concentrations. 1,25(OH)2D increased incrementally from baseline levels of 34 +/- 3(SE) pg/ml to 39 +/- 3 pg/ml (P = 0.2) with low-grade estrogen stimulation and to 43 +/- 3 pg/ml (P less than 0.05) with medium-grade estrogen stimulation, while 25(OH)D, 24,25(OH)2D, vitamin D binding protein, parathyroid hormone, calcium, and phosphate did not change. 24,25(OH)2D was correlated to 25(OH)D at baseline (r = 0.65, P less than 0.01) and with low-grade estrogen stimulation (r = 0.62, P less than 0.01), but not with medium-grade stimulation (r = 0.13); these relationships are consistent with the concepts that 25(OH)D is metabolized predominantly to 24,25(OH)2D at low estrogen levels, but not at higher estrogen levels. We conclude that endogenous estrogen elevation promotes formation of 1,25(OH)2D from 25(OH)D, and that it may reciprocally inhibit synthesis of 24,25(OH)2D.

24,25-Dihydroxyvitamin D 3↗
PubMed1987

Effects of vitamin D3, 25-hydroxyvitamin D3, and 24,25-dihydroxyvitamin D3 on parathyroid hormone secretion.

The active vitamin D metabolite 1,25-dihydroxyvitamin D3 [1,25(OH)2D3] causes marked suppression of both pre-proparathyroid hormone messenger RNA (pre-proPTH mRNA) and parathyroid hormone (PTH) secretion. These effects are dose dependent and reversible when tested in an in vitro primary tissue culture cell system using normal bovine parathyroid cells. In the current studies, the precursors of 1,25(OH)2D3 and the related metabolite 24,25-dihydroxyvitamin D3 [24,25(OH)2D3], were used in the same culture system to test for possible regulatory effects. The results were compared with identically prepared cells exposed to 1,25(OH)2D3. In short-term studies (30-120 minutes), none of the vitamin D-related compounds produced any effect on PTH secretion. In long-term studies (24-48 hours, using primary tissue culture in the presence of test agents), neither vitamin D3 nor 25(OH)D3 affected PTH secretion or pre-proPTH mRNA over the concentration range 10(-11)-10(-7) M. On the other hand, 24,25(OH)2D3 produced significant suppression of both pre-proPTH mRNA (77% of control, P less than .01) and PTH secretion (75% of control, P less than .005) at 10(-7) M. By comparison, 10(-11) M 1,25(OH)2D3 produced levels of suppression (25-30%) of both pre-proPTH mRNA and PTH secretion comparable to 10(-7) M 24,25(OH)2D3, while even greater suppression (40-50%) occurred at 10(-9)-10(-7) M 1,25(OH)2D3. From these studies, we conclude that vitamin D3 and 25(OH)D3 do not have significant effects on PTH synthesis and secretion over the range of doses tested.(ABSTRACT TRUNCATED AT 250 WORDS)

24,25-Dihydroxyvitamin D 3↗
PubMed1988

Effect of vitamin D status on the activity of carbonic anhydrase in chicken epiphysis and kidney.

Chickens were raised for 6 weeks from the date of hatch under red light on a vitamin D-free diet; controls were given an oral vitamin D supplement. Vitamin D-deficient animals showed decreased total serum calcium concentration and decreased DNA content in epiphysis and kidney homogenates. In calcifying epiphysis, total carbonic anhydrase (CA) activity was decreased, but activity per microgram DNA was slightly increased and specific activity was double that of the controls. Polyacrylamide gel isoelectric focusing after preparation of the enzyme showed a picture similar to that seen after parathyroid hormone (PTH) administration in chicks; therefore, this could be considered a secondary hyperparathyroidism. The CA activation was not seen in the kidney which can be explained by induction of an endogenous inhibitor protein of the cyclic AMP-dependent protein kinase exclusively in the kidney in vitamin D deficiency. In an additional experiment, chickens were raised for 3 weeks from the date of hatch under red light on a vitamin D-free diet. Daily oral substitution by different vitamin D metabolites (1,25(OH)2D3, 25OHD3, 24,25(OH)2D3) over 7 days led to CA activation compared with controls probably by restoring protein kinase activity in the kidney. Our results show that CA activity is inversely correlated with serum calcium concentrations which is in agreement with a regulatory mechanism recently proposed by us.

24,25-Dihydroxyvitamin D 3↗
PubMed1986

Vitamin D3 and avian bone in vitro: specificity of effect on Japanese quail calvaria.

Calcitriol (1,25(OH)2D3) has been shown, under certain conditions, to elicit an in vitro response in adult avian calvarium which may be interpreted as calcium uptake by the bone. The present investigation was undertaken to study the specificity of this response. Calvaria were removed from 6-week-old female Japanese quail and cultured for periods of up to 96 hours at 37 degrees C in 5% CO2/95% air. 1,25(OH)2D3 induced a fall in the medium total and ionic calcium concentrations at both 48 hours and 96 hours of incubation; these responses were not blocked by the presence of 10(-4) M acetazolamide. Bovine parathyroid hormone (bPTH(1-34] at 10(-7) M, and dibutyryl cyclic AMP (DBcAMP) at 10(-4) M, had no effect on the medium calcium. In contrast, forskolin at 10(-4) M induced a marked fall in medium calcium concentrations, particularly at 48 hours. The specificity was also studied with respect to vitamin D3 and its two major metabolites. 1,25(OH)2D3 exhibited a bell-shaped dose-response relationship with the maximal effect at 10(-7) M. In contrast, the other two compounds elicited no effects at 10(-7) M or 10(-6) M; significant responses were observed at 10(-5) M with both agents. In general, 25-dihydroxyvitamin D3 (25OHD3) was more potent than vitamin D3. These findings suggest that the medium calcium response to 1,25(OH)2D3, interpreted as calcium uptake by the cultured adult avian bone, is relatively specific among calcemic agents; the response was elicited by forskolin but not by bPTH(1-34) or DBcAMP.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetazolamide↗