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PubMed1981

Autoradiographic studies with 3H 1,25 (OH)2 vitamin D2 and 3H 25 (OH) vitamin D3 in rat parathyroid glands.

After injection of radiolabeled 1,35 (OH)s vitamin D3, nuclear concentration of radioactivity is observed in parenchymal cells o hte parathyroid gland in pregnant, adult male, and 10-day male neonatal rats. In competition studies with unlabeled 1,25 (OH)2 vitamin D3, but not with 25 (OH) vitamin D3, in contrast to 3H 1,25 (OH)2 vitamin D3, do not show nuclear concentration in cells of te parathyroid. The results of te autoradiographic studies suggest the presence of receptors for a direct effect of 1,35 (OH)2 vitamin D3 on the parathyroid gland for modulation of parathyroid hormone secretion.

Aging↗

PubMed1993

Affinity differences for vitamin D metabolites associated with the genetic isoforms of the human serum carrier protein (DBP).

Human vitamin D binding protein (DBP) displays considerable polymorphism with 120 described alleles. Among these, three alleles are frequently observed, Gc 1F (pI 4.94-4.84), Gc 1S (pI 4.95-4.85) and Gc 2 (pI 5.1). Differences between these genetic forms of the protein in affinity for vitamin D metabolites have been detected by electrophoretic methods. The constant affinity (Ka) values determined in this study confirm these differences. The affinities of six rare variants were also examine. Those of the DBP genetic forms to the vitamin D derivatives 25-OH-D3 and 1,25-(OH)2-D3 seem to be related to the isoelectric point of the proteins: a high affinity corresponding to a low isoelectric point. The Gc 1A9 and 1A11 mutants were associated with higher affinity for the vitamin D derivatives and the Gc 1C1 and 1C21 mutants were deficient.

Calcifediol↗

PubMed1985

Plasma concentrations of vitamin D metabolites during puberty of diabetic children.

Plasma concentrations of 25-hydroxyvitamin D, 1,25-dihydroxyvitamin D, 24,25-dihydroxyvitamin D and vitamin D binding protein were determined in 87 serum samples from 46 Type 1 (insulin-dependent) diabetic children and adolescents at the various stages of puberty. The results were compared with data similarly obtained from healthy pubertal children. The diabetic patients had lower mean 1,25-dihydroxyvitamin D concentrations (p less than 0.05) and higher molar ratios of 24,25-dihydroxyvitamin D to 25-hydroxyvitamin D (p less than 0.05) than their healthy counter parts. In contrast to the reference group, the diabetic patients failed to attain the increase in 1,25-dihydroxyvitamin D normally seen during the pubertal stages of maximal growth velocity. The mean plasma levels of vitamin-D binding protein did not differ between the two groups, and a calculated 'free' 1,25-dihydroxyvitamin D value followed a pattern similar to that of total 1,25-dihydroxyvitamin D throughout puberty for both groups. The results suggest that the regulatory mechanisms of the vitamin D endocrine system are altered in diabetic children at puberty, resulting in a relative decrease in 1,25-dihydroxyvitamin D plasma concentration and increased 24,25-dihydroxyvitamin D levels.

24,25-Dihydroxyvitamin D 3↗

PubMed1992

Serum intact parathyroid hormone levels in elderly Chinese females with hip fracture.

Serum intact parathyroid hormone (PTH), 25 hydroxyvitamin D(25OHD), 1,25 dihydroxyvitamin D (1,25(OH)2D), albumin, and ionized calcium were measured in 61 Chinese female patients with hip fracture and 61 control subjects. Hip fracture patients had low albumin, ionized calcium, and 250HD levels. Serum PTH and 1,25(OH)2D values were not different between the two groups. We conclude that although 250HD level in hip fracture patients is low, there is no evidence of secondary hyperparathyroidism, suggesting that the low 250HD levels may be a secondary phenomenon in response to the fracture.

Aged↗

PubMed1995

Increased bone resorption and decreased bone formation in Chinese patients with hip fracture.

Biochemical markers of bone formation (bone-specific alkaline phosphatase and osteocalcin) and bone resorption (hydroxyproline excretion and bone isoenzyme of acid phosphatase) were measured in 30 patients (15 M and 15 F) with hip fracture and 30 healthy subjects matched for age and sex. Bone isoenzyme of tartrate-resistant acid phosphatase (TRACP) was measured by a recently developed specific immunoassay. Serum osteocalcin concentration and bone-specific alkaline phosphatase activity were significantly lower and serum TRACP concentration and urinary hydroxyproline excretion were elevated in patients compared with healthy subjects. We suggest that there is reduced bone formation and increased bone resorption in patients with hip fracture.

Acid Phosphatase↗

PubMed1994

Relations between calcidiol serum levels and bone mineral density in postmenopausal women with low bone density.

The relationship between vitamin D and bone density was studied in 150 selected, mature (45-74), postmenopausal women with a lumbar spine Z score below 0. Vitamin D status was evaluated using calcidiol serum levels. Serum calcitriol and parathyroid hormone (PTH) values were also evaluated in some subjects. Bone mass was evaluated by ascertaining bone density and Z and T scores in the lumbar spine and femur region. The reference group consisted of 25 premenopausal women. The postmenopausal group was divided into subgroups according to age, i.e., under or over 60 years old. Additionally, the whole group was also subdivided according to their lumbar spine Z scores into group I (Z > -1), group II (Z < -1; > -2), and group III (Z < -2). Group III of postmenopausal women had higher PTH and lower calcitriol levels than premenopausal women. Calcidiol serum levels were lower in postmenopausal women groups II or III than in the group I and premenopausal women. Calcidiol serum levels and the bone mass values for the lumbar spine were correlated positively in all the postmenopausal women; in the women over 60 years of age, calcidiol levels also correlated with the bone mass values expressed as the bone density in three femur regions: femoral neck, trocanter, and Ward's triangle. In conclusion, mature post-menopausal woman showed high PTH levels and low calcidiol and calcitriol values. Calcidiol status is significantly related to bone mineral density in the lumbar spine and in women over 60 years, calcidiol levels also correlated with bone density in the femur regions.

Adult↗

PubMed1992

Menopausal bone loss is partially regulated by dietary intake of vitamin D.

Five years ago we reported results from a cross-sectional study of the effect of nutritional factors on calcium-regulating hormones and bone loss in perimenopausal women. We found an inverse correlation between serum 25-hydroxyvitamin D (25OHD) and immunoreactive parathyroid hormone (PTH), and we postulated that over time, women with lower 25OHD would lose more bone because of increased bone remodeling induced by secondary hyperparathyroidism. We have followed 38 of these women for 5 years. Twenty-two have gone through menopause and we are reporting observations on these 22 subjects. Bone mineral analysis was performed twice a year at the distal and mid-radius using single-photon absorptiometry. The slope of the bone mineral content curve was calculated by least squares. Bone loss increased within 6 months of the rise in serum follicle stimulating hormone (FSH) to greater than 40 mIU/ml. We continued to see a negative correlation between 25OHD and PTH (r = -0.450, P = 0.03). Premenopause, PTH was negatively correlated with the proximal bone mineral content (PBMC) slope (-0.604, P = 0.002). The distal bone mineral content (DBMC) 5-year slope was correlated with dietary vitamin D (r = 0.509, P = 0.02), the higher the intake, the less negative the slope. The 5-year PBMC slope was negatively correlated with serum osteocalcin (OC) levels (r = -0.382, P = 0.08). Before menopause, the change in PBMC was positively correlated with OC (r = 0.450, P = 0.03). Postmenopause, the correlation with DBMC slope was negative (r = -0.506, P = 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

25-Hydroxyvitamin D 2↗

PubMed1989

The in vivo and in vitro effect of calmodulin antagonists on the renal actions of 25(OH) vitamin D3 in the rat.

Previous work from this laboratory has demonstrated that 25(OH) vitamin D3 [25(OH)D3] acutely suppresses the phosphaturic action of parathyroid hormone (PTH) and interferes with the PTH-induced activation of adenylate cyclase (AC). Calmodulin inhibitors block vitamin D-induced Ca2+ transport in the gut and phosphorus uptake in renal BBMV's. We have examined whether calmodulin antagonists affect the renal action of 25(OH)D3. Acute clearance experiments were performed in PTH-infused parathyroidectomized rats receiving 25(OH)D3 after pretreatment with trifluoperazine (TFP) or promethazine (P). In vitro PTH-induced activation of renal AC was also studied in membrane preparations from pretreated rats in the presence of 25(OH)D3. 25(OH)D3 reduced the PTH-stimulated increase in fractional excretion of phosphorus (CP/CIn) from 0.292 +/- 0.024 to 0.195 +/- 0.018 (p less than 0.005) and urinary cAMP from 149.3 +/- 20.3 to 78.1 +/- 10.4 pmol/min (p less than 0.01) and also blunted AC activation in vitro. TFP but not P abolished the effects of 25(OH)D3 both in vivo and in vitro. R 24571 also abolished the in vitro effect of 25(OH)D3. Thus, (1) TFP abolishes both the antiphosphaturic and the AC/cAMP-related actions of 25(OH)D3, (2) P does not have these effects, and (3) R 24571 abolishes the in vitro effect of 25(OH)D3. These results suggest that the antiphosphaturic effect of 25(OH)D3 acting via the AC/cAMP system may be calmodulin dependent.

Adenylyl Cyclases↗

PubMed1990

Serum vitamin D metabolites in cadmium-exposed persons with renal damage.

Serum concentrations of 25-hydroxyvitamin D [25(OH)D], 24,25-dihydroxyvitamin D [24,25(OH)2D], and 1 alpha,25-dihydroxyvitamin D [1 alpha,25(OH)2D] were measured in ten cadmium (Cd)-exposed subjects and five non exposed subjects. The Cd-exposed subjects were divided into two groups according to serum 1 alpha,25(OH)2D levels. No significant differences for 25(OH)D were found between the Cd-exposed group with low or normal serum 1 alpha,25(OH)2D and the non exposed group. The concentrations of 24,25(OH)2D were the lowest in the Cd-exposed group with low serum 1 alpha,25(OH)2D, highest in the non exposed group, and significantly lower in the Cd-exposed group with normal serum 1 alpha,25(OH)2D than in the non exposed group. Renal function was much worse in the Cd-exposed group with low serum 1 alpha,25(OH)2D than in the group with normal serum 1 alpha,25(OH)2D. These findings indicate that Cd initially disturbs hydroxylation from 25(OH)D to 24,25(OH)2D and then disturbs hydroxylation from 25(OH)D to 1 alpha,25(OH)2D. The decrease of serum 24,25(OH)2D and 1 alpha,25(OH)2D in Cd-exposed subjects is not due to a decrease of the serum 25(OH)D level.

24,25-Dihydroxyvitamin D 3↗

PubMed1990

Blood levels of active metabolites of vitamin D3 in fracture repair in humans. A preliminary report.

Blood levels of the active metabolites of vitamin D3, 25-hydroxycholecalciferol [25(OH)D3], 1,25-dihydroxycholecalciferol [1,25(OH)2D3] and 24,25-dihydroxycholecalciferol [24,25(OH)2D3] were determined in seven patients. Two subjects suffered from delayed union of tibial fractures; one showed a delayed union after a proximal tibial osteotomy; one patient suffered from bilateral femoral neck fractures, of which one failed to unite and the other united late; two patients had multiple fractures that united normally; and one patient exhibited staged bilateral femoral neck fractures whose occurrence was separated by a short interval and which united without undue delay. The blood levels of 25(OH)D3 were within the normal range. A relative decrease in 24,25(OH)2D3 values was noted in all patients, whereas in three subjects the decrease was absolute, to non-detectable levels. A decrease in 1,25(OH)2D3 levels was noted in only two patients. We postulate that these changes reflect the consumption of these metabolites during healing at the fracture site.

24,25-Dihydroxyvitamin D 3↗

PubMed1995

Glucose intolerance and impairment of insulin secretion in relation to vitamin D deficiency in east London Asians.

Vitamin D deficiency reduces insulin secretion and still occurs in East London Asians in whom the prevalence of diabetes mellitus is at least four times that of Caucasians. Vitamin D status was assessed in 44 of 65 non-diabetic subjects 'at risk' of diabetes (spot blood glucose level >6.0 mmol/l <2 h post cibum, or>4.6 mmol/l >2 h post cibum on two separate occasions) and in 15 of 60 age and sex-matched 'low-risk' control subjects who attended for oral glucose tolerance test (OGTT) after screening of 877 omnivorous subjects not known to have diabetes. It was found that 95% of at-risk and 80% of low-risk subjects were vitamin D deficient (serum 25-hydroxy-vitamin D <11 ng/ml). Diabetes was present in 16, impaired glucose tolerance in 12 and normoglycaemia in 19 at-risk subjects, imparied glucose tolerance in 2, and normoglycaemia in 13 low-risk subjects. Correlation of 30-min OGTT blood glucose, specific insulin and C-peptide levels with 25-hydroxy-vitamin D concentrations in 44 at-risk subjects were -0.31 (p=0.04), 0.59 (p=0.0001) and 0.44 (p=0.006). In 15 'not-at-risk' subjects 30-min OGTT specific insulin and C-peptide levels correlated with 25-hydroxy-vitamin D, r=0.39 (p=0.04) and 0.16 (p=0.43), respectively. Serum alkaline phosphatase concentration was higher in at-risk than not-at-risk subjects (59.6 vs 46.5 IU/l, p=0.012); corrected calcium concentrations were comparable (2.38 vs 2.39 mmol/l, p=0.7). Following treatment with 100,000 IU vitamin D by i.m. injection, specific insulin, C-peptide [30 min on OGTT] and 25-hydroxy-vitamin D concentrations had risen 8-12 weeks later [mean +/- DS] from 57 +/- 62 to 96.2 +/- 82.4 mU/l [p=0.0017], 1.0 +/- 0.4 to 1.7 +/- 0.8 pmol/ml [p=0.001] and 3.6 +/- 1.8 to 13.5 +/- 7.4 ng/ml [p=0.0001], (but not to low-risk group values of 179 +/- mU/l, 2.7 +/- 1.14 pmol/ml and 8.16 +/- 6.4 ng/ml), respectively. Both total serum alkaline phosphatase and corrected calcium concentrations rose following vitamin D treatment in the at-risk subjects by 11.1 +/- 8.22 (from 44 to 55 IU/l) and 0.15 +/- 0.18, (2.43 to 2.57 mmol/l), respectively (p=0.004). Abnormal glucose tolerance was unchanged by vitamin D treatment. The value of early and sustained repletion with vitamin D in diabetes prophylaxis should be examined in communities where vitamin D depletion is common.

Asian People↗

PubMed1985

High incidence of low serum vitamin D concentration in patients with hip fracture.

The study of 82 consecutive hip fracture patients (22 males and 60 females) and 185 various controls showed that low serum 25-OH-vitamin D3 (25-OD-D3) concentration was common in the hip fracture patients, who in addition were old, incapable of independent daily life, had poor dietary habits, reduced nutritional status, and spent insufficient time in sunlight. The most usual mechanisms of trauma were minor indoor falls. Osteoporosis was common and associated with low 25-OH-D3. Hypocalcemia was more common in hip fracture patients than in controls. Increased serum alkaline phosphatase was not a specific feature in hip fracture patients. The results suggest that vitamin D supplementation is indicated in elderly disabled people.

Adult↗

PubMed1989

25 Hydroxyvitamin D and vitamin E absorption in healthy children and children with chronic intrahepatic cholestasis.

Patients with chronic cholestasis have reduced 25-hydroxyvitamin D (25OHD) and vitamin E levels. We determined serum concentrations of 25OHD, 1,25-dihydroxyvitamin D [1,25(OH)2D] and vitamin E before and after oral administration of 10 micrograms/kg body weight 25-hydroxyvitamin D3 (25OHD3) and 100 IU/kg body weight vitamin E, respectively, in 4 patients with intrahepatic cholestasis and 6 healthy children. Vitamin E increased in all controls but in only one of the four patients. In contrast, oral 25OHD3 induced a normal rise in circulating 25OHD and 1,25(OH)2D. The low serum levels of 25OHD in the patients before the oral bolus may have been due to inadequate parenteral vitamin D administration and/or to the simultaneous phenobarbital treatment. The latter possibility is supported by the increase of serum 25OHD into the normal range after withdrawal of phenobarbital in one of the four patients. We conclude that vitamin E has to be supplemented parenterally or in water-soluble oral form. Further studies are necessary to clarify whether high-dose long-term oral 25OHD3 supplementation is sufficient to prevent vitamin D deficiency in patients with chronic cholestasis.

Adolescent↗

PubMed1986

Decreased bone density in severely handicapped children and adults, with reference to the influence of limited mobility and anticonvulsant medication.

Bone density and related biochemical parameters were investigated in institutionalised children and adults with severe handicaps, who were classified according to the degree of limited mobility (group 1, bed-ridden; group 2, capable of crawling; group 3, capable of walking) and according to whether or not they were receiving anticonvulsants. As determined by microdensitometric analysis of radiograms of the second metacarpal bone, bone width (D), bone pattern area (sigma GS) and bone salt density (sigma GS/D) were decreased in the patients, the decreases being most prominent in group 1, followed by groups 2 and 3, in that order. Significant decreases of sigma GS and sigma GS/D, but not of D, were found in patients on anticonvulsant treatment in comparison to patients without therapy. Serum alkaline phosphatase (Al-p) and parathyroid hormone (iPTH) as well as urinary calcium and cyclic adenosine-3',5'-monophosphate (cAMP) excretion were significantly increased in group 1. In comparison to patients without therapy, anticonvulsant-treated children showed significantly decreased levels of serum calcium (Ca), ionised Ca (Ca2+), 25-hydroxy vitamin D3 and urinary phosphate (PO4) excretion, and elevated levels of Al-p, iPTH and calcitonin (iCT). It is suggested that limited physical activity results in a mild hyperparathyroid state, which is aggravated in patients on anticonvulsant treatment.

Adolescent↗

PubMed1986

Parathyroid hormone, calcitonin and vitamin D metabolites in beta-thalassaemia major.

Serum calcium (Ca), phosphorus (P), alkaline phosphatase (Al-P), parathyroid hormone (PTH), calcitonin (CT), 25-hydroxyvitamin D3 (25OHD3), 1,25-dihydroxyvitamin D3 (1,25(OH)2D3) levels and urinary excretion of Ca, P, hydroxyproline (OH-P) and cyclic AMP (cAMP) were determined in summer and in winter in 13 thalassaemic children (7 aged 3-5 years-group 1-; and 6 aged 10-13 years-group 2-), who had never taken vitamin D supplements or therapy, and in two groups of 14 controls of the same age. In thalassaemics of group 1 only serum Al-P levels and OH-P urinary excretion were higher than in controls (P less than 0.01). In thalassaemics of group 2 Ca (P less than 0.05), P (P less than 0.05), PTH (P less than 0.001), CT (P less than 0.001), 25OHD3 (P less than 0.05), 1,25(OH)2D3 (P less than 0.001) levels and cAMP urinary excretion (P less than 0.001) were lower, whereas Al-P (P less than 0.001) and CT (P less than 0.001) levels and urinary excretion of P (P less than 0.05) and of OH-P (P less than 0.001) were higher than in controls, both in summer and in winter. Advancing age induces in thalassaemic patients a decrease in PTH secretion and a consequent deficit in synthesis of 1,25(OH)2D3 that may explain some aspects of bone changes, which CT hypersecretion may tend to counteract.

Adolescent↗

PubMed1988

Evidence that calcitonin plays a role in the postnatal increase of serum 1 alpha,25-dihydroxyvitamin D.

To investigate the changes in the 1 alpha,25-dihydroxyvitamin D [1,25(OH)2D] level and the role of parathyroid hormone (PTH) and calcitonin (CT) during the early neonatal periods, we measured 1,25(OH)2D, 25-hydroxyvitamin D [25(OH)D], PTH specific for mid-regions (mPTH) and urinary cAMP (UcAMP) to evaluate the renal tubular responsiveness to intrinsic PTH and CT, as well as serum Ca and P in 28 mothers at term delivery and in their babies at birth and 5 days of age. Cord serum 1,25(OH)2D levels were low (28.8 +/- 9.2 pg/ml, mean +/- SD), while maternal serum 1,25(OH)2D levels were high (62.2 +/- 22.6 pg/ml). The low 1,25(OH)2D value increased 2.5 times (62.2 +/- 22.6 pg/ml) in 5-day-old infants, reaching a high normal adult value, concomitant with the increases in mPTH and urinary cAMP/creatinine ratio (UcAMP/Cr). The correlations between 1,25(OH)2D and UcAMP/Cr, and 1,25(OH)2D and mPTH in all paired samples of babies at birth and at 5 days of age were r = 0.456, n = 50, P less than 0.01 and r = 0.341, n = 50, P less than 0.05, respectively. These data suggest that the parathyroid activation after birth is a major factor in the rapid 1,25(OH)2D increment at that time. CT levels were high in all paired samples and in 5-day-old infants. CT vs 1,25(OH)2D showed a significant correlation (r = 0.473, P less than 0.05, n = 24) as well as the relative increase of 1,25(OH)2D (delta pg/ml) after birth vs CT at age 5 days (r = 0.537, P less than 0.01, n = 24).(ABSTRACT TRUNCATED AT 250 WORDS)

Calcifediol↗

PubMed1987

The increase in skin 7-dehydrocholesterol induced by an hypocholesterolemic agent is associated with elevated 25-hydroxyvitamin D3 plasma level.

Vitamin D3 is generated in skin by UV irradiation of 7-dehydrocholesterol (7-DEHC). Whether the 7-DEHC amount in skin affects vitamin D3 formation, and thereby the plasma level of 25-hydroxyvitamin D3 (25[OH]D3) is not known. In the present work we report on the influence on vitamin D and Ca metabolism of a new hypocholesterolemic agent, HCG-917 (0-2-[hydroxy-3-]N'-(2-chlorophenyl)-N-piperazinyl-1- [propyl]-4-chloro-benz-aldoxim-hydrochloride) which inhibits 7-DEHC reductase and thereby increases skin 7-DEHC. Rats were treated with HCG 917 (0.3 and 5.0 mg/kg, orally) for 13 days. HCG 917 caused a dose-dependent decrease in cholesterol and concomitant accumulation of 7-DEHC in plasma and skin. In skin, 7-DEHC was: control: 1.05 +/- 0.20; HCG 917, 0.3 mg/kg: 1.41 +/- 0.22; HCG 917, 5.0 mg/kg: 2.35 +/- 0.35 mg/g. At a dose of 0.3 mg/kg, HCG 917 had no significant influence on the plasma level of neither 25(OH)D3 nor 1,25(OH)2D3. However, at a dose of 5.0 mg/kg, HCG 917 induced a significant increase in plasma 25(OH)D3 (control: 36.2 +/- 2.2; HCG 917 5.0 mg/kg: 57.6 +/- 6.5 nmol/l) and a slight but not significant rise in 1,25(OH)2D3. Calcium balance studies indicated that HCG 917 did not influence intestinal Ca absorption nor urinary Ca excretion. At a dose of 5.0 mg/kg HCG 917 slightly induced a decrease in total plasma Ca. In conclusion, HCG 917 treatment can induce a significant rise in skin 7-DEHC with an increase in plasma 25(OH)D3. These results suggest that variation in the skin level of 7-DEHC can directly influence the cutaneous production of vitamin D3 and thereby the vitamin D status of the organism.

Animals↗

PubMed1989

Rapid stimulation of calcium uptake by isolated rat enterocytes by 1,25(OH)2D3.

Evidence is accumulating that 1,25(OH)2D3 may stimulate calcium transport from the intestinal lumen extremely rapidly by a mechanism which appears independent of de novo protein synthesis. To investigate this rapid action of 1,25(OH)2D3, the rate of calcium uptake by isolated enterocytes from duodena of young rats was determined in vitro as the uptake of 45Ca from 1-15 min. Prior in vitro exposure of cells to 1,25(OH)2D3 (100 pM) for 20 min significantly increased the rate of calcium uptake (p less than 0.001), an effect unaltered by 50 microM cycloheximide. Incubation with 100 pM 1-alpha-hydroxyvitamin D3 produced the same effect (p less than 0.01). In contrast, exposure to 10 pM 1,25(OH)2D3, as well as to 100 pM or to 1,000 pM 25-hydroxyvitamin D3 induced no significant change. Because both 1,25(OH)2D3 and starvation may stimulate key enzymes in polyamine metabolism, we investigated the effects of (i) difluoromethyl-ornithine (CHF2-Orn), a specific irreversible inhibitor of ornithine decarboxylase and (ii) varying the timing of feeding prior to sacrifice. Both in vitro CHF2-Orn and feeding prior to sacrifice significantly decreased the baseline rate of calcium uptake (p less than 0.05) and reduced the effect of 1,25(OH)2D3. Increased duration of starvation significantly increased the baseline rate of calcium uptake (p less than 0.02) without changing the increment in rate of calcium uptake induced by 1,25(OH)2D3. The study suggests (i) that the early action of 1,25(OH)2D3 on the influx process of intestinal calcium transport may involve a different molecular specificity from that involved in the genomic action of 1,25(OH)2D3 and (ii) that changes in polyamine metabolism may play a part in this process.

Animals↗