Effects of 1αOHD2 on bone tissue Studies of 1αOHD2 and 1αOHD3 in normal rats and in rats treated with prednisolone

1984 ◽  
Vol 106 (4) ◽  
pp. 564-568 ◽  
Author(s):  
G. O.J. Sjödén ◽  
O. Johnell ◽  
H. F. DeLuca ◽  
J. U. Lindgren

Abstract. Three months old male rats were fed a diet containing 0.3% calcium and 0.5% phosphate. Prednisolone was added to the diet at a dose of 1.5 mg a day and the effect of oral treatment with 0.5 μg 1αOHD2 or 0.5 μg 1αOHD3 was studied. After 6 weeks rats given prednisolone had a lower bone mass and bone density. The serum phosphate concentration was also lower. Rats given 1αOHD3 had an increased serum calcium concentration even when simultaneously treated with prednisolone. 1αOHD2 did not cause hypercalcaemia. The decrease in bone density caused by prednisolone was prevented by the administration of 1αOHD2. Rats receiving 1αOHD3 together with prednisolone still exhibited a lower bone density. Furthermore, 1αOHD3 decreased bone mass in normal rats and caused a higher mean value of osteoclasts/area whereas 1αOHD2 reduced the number of osteoclasts/area. The study indicates that 1αOHD2 is an effective vitamin D analogue with a lower tendency to cause bone resorption.

PEDIATRICS ◽  
1974 ◽  
Vol 53 (3) ◽  
pp. 404-409
Author(s):  
Betty S. Roof ◽  
Carolyn F. Piel ◽  
Linda Rames ◽  
Donald Potter ◽  
Gilbert S. Gordan

Circulating radioimmunoassayable parathyroid hormone (iPTH) was not present in 30% (117) of 389 normal children tested at ages from cord blood to 17 years. In the other 70% (272), mean iPTH was found to be 25 ± 0.7µl eq/ml (± SEM; range, 0-53 ± 2 SD) . The iPTH levels were elevated in 59% of 24 uremic children without radiologic evidence of osteodystrophy in 94% uremic children with osteodystrophy. Infusion of calcium (10 mg/kg over three hours or 15 mg/kg over four hours) in the children without osteodystrophy reduced the iPTH by nearly 50%; suppression was sustained for 9 to 20 hours. In uremic children with osteodystrophy, similar infusions failed to elevate the serum calcium concentration to the same degree and there was less suppression of iPTH which was not sustained as long. Mean increment in serum calcium observed was 2.1 mg/100 ml with 10 mg/kg/3 hr and 3.4 for 15 mg/kg/4 hr in children without osteodystrophy, and 1.24 and 1.4 mg/100 ml in those with osteodystrophy for similar infusions. In both groups, calcium infusions lowered the concentration of serum magnesium and elevated the serum phosphate concentration. Tubular reabsorption of phosphate did not change consistently despite fall in serum iPTH levels. There was no correlation between suppressibility of parathyroid function and serum creatinine level. In five children with osteodystrophy in whom calcium infusions did not suppress iPTH levels, normal iPTH levels were achieved rapidly after successful renal transplantation. These data indicate that the secondary hyperparathyroidism of uremic children is suppressible and not autonomous.


2012 ◽  
Vol 64 (4) ◽  
pp. 1585-1589
Author(s):  
M. Focak ◽  
E. Haskovic ◽  
D. Suljevic

The effect of fluoride on the calcium level in serum was analyzed in the laboratory rat Rattus norvegicus. The control group consisted of 10, and the experimental group of 15 animals. In the experimental group, fluoride at a concentration of 3 mg/100 g body weight of rats was intramuscularly injected into the musculus gluteus maximus. The concentration of calcium was measured by the CPC method. The average serum calcium concentration was 2.46 mmol/l, with female rats having higher values of serum calcium than male rats. Fluoride caused the reduction of calcium concentration in serum (p<0.05); the reduction was significantly expressed in female rats (p<0.000).


1972 ◽  
Vol 70 (3) ◽  
pp. 476-486 ◽  
Author(s):  
S. Pors Nielsen ◽  
F. Schønau Jørgensen

ABSTRACT Subcutaneous injection of 300 μmol magnesium raised the serum magnesium to 4.00 mmol/l after 30 min in 150 g male rats and reduced the serum calcium concentration by 0.17 mmol/l after 60 min. Magnesium also acutely diminished the serum concentration of 45Ca given three weeks previously. The administration of magnesium did not reduce the serum concentration of 45Ca and did not increase the rate of disappearance of 45Ca from the serum, when subcutaneous or intravenous labelling took place 180–210 min before the magnesium injection. The magnesium-induced hypocalcaemia therefore cannot be explained by an increased removal of calcium from the circulation. The results are compatible with the hypothesis that the magnesium-induced hypocalcaemia is caused by the release of calcitonin. Injections of 300 μmol magnesium chloride at 12 h intervals for 72 h trebled the 24 h renal excretion of both 40Ca and 45Ca given three weeks previously. The 24 h renal excretion of hydroxyproline was unaltered. Thus there was no indication that the intermittent magnesium injections produced any long-term inhibition of the turnover of bone matrix and bone mineral.


Bone ◽  
2018 ◽  
Vol 116 ◽  
pp. 162-170 ◽  
Author(s):  
Emily E. Hohman ◽  
Joanna K. Hodges ◽  
Meryl E. Wastney ◽  
Pamela J. Lachcik ◽  
Chun-Ya Han ◽  
...  

1985 ◽  
Vol 63 (8) ◽  
pp. 978-982 ◽  
Author(s):  
M. Warner ◽  
A. Tenenhouse

The regulation of renal mitochondrial 1-hydroxylase activity in chronic vitamin D deficiency was studied in male rats. These rats were born of mothers who had been raised from weaning (21 days) on a vitamin D deficient diet and who had no detectable serum 1,25-dihydroxycholecalciferol (1,25-(OH)2D) at the time their offspring were weaned (28 days). In the pups, renal mitochondrial 1-hydroxylase activity was undetectable before the 3rd week of life even though the animals were severely hypocalcemic from birth. The 1-hydroxylase activity first became detectable at 26 days of age, rapidly reached a maximum at day 34, then decreased to become undetectable again by 65 days. Throughout this time serum calcium concentration was <5.0 mg/dL and serum parathyroid hormone (PTH) concentration, measured by a midmolecule radioimmunoassay, was two-to five-fold greater than that found in vitamin D replete rats. 1-Hydroxylase activity could be restored in the +65-day-old animals by administration of a single dose of 2.5 μg vitamin D3. Enzyme activity was detected within 24 h, was maximal at 72 h, and returned to undetectable levels by 96 h after administration of the vitamin. Serum 1,25-(OH)2D which was undetectable before administration of the vitamin D3, was 108 and 458 pg/mL at 16 and 40 h, respectively, after the injection. The serum concentration of this metabolite then decreased progressively to 80 pg/mL by 6 days. 24-Hydroxylase activity first became detectable 48 h after vitamin D administration, increased to a maximum at 96 h, and thereafter decreased to become undetectable by 7 days. The urinary excretion of phosphate and cyclic AMP was 10% of control values between 65 and 90 days of age. These values became normal 4 days after a single dose of 2.5 μg vitamin D3. From these data it is concluded that there are two distinct levels of regulation of 1-hydroxylase activity: a vitamin D independent induction of the activity at the time of weaning that is transient and is not associated with any detectable 24-hydroxylase activity; and the second is a vitamin D dependent induction of enzyme activity seen in animals which prior to administration of the vitamin manifest the characteristics of PTH resistance and have no detectable renal hydroxylase activity. The mechanisms of these effects remain to be determined.


Endocrinology ◽  
1968 ◽  
Vol 83 (6) ◽  
pp. 1375-1376 ◽  
Author(s):  
BERNARD F. RICE ◽  
ROY PONTHIER ◽  
M. CLINTON MILLER

PEDIATRICS ◽  
1990 ◽  
Vol 86 (3) ◽  
pp. 440-447 ◽  
Author(s):  
Laura K. Bachrach ◽  
David Guido ◽  
Debra Katzman ◽  
Iris F. Litt ◽  
Robert Marcus

Osteoporosis develops in women with chronic anorexia nervosa. To determine whether bone mass is reduced in younger patients as well, bone density was studied in a group of adolescent patients with anorexia nervosa. With single- and dual-photon absorptiometry, a comparison was made of bone mineral density of midradius, lumbar spine, and whole body in 18 girls (12 to 20 years of age) with anorexia nervosa and 25 healthy control subjects of comparable age. Patients had significantly lower lumbar vertebral bone density than did control subjects (0.830 ± 0.140 vs 1.054 ± 0.139 g/cm2) and significantly lower whole body bone mass (0.700 ± 0.130 vs 0.955 ± 0.130 g/cm2). Midradius bone density was not significantly reduced. Of 18 patients, 12 had bone density greater than 2 standard deviations less than normal values for age. The diagnosis of anorexia nervosa had been made less than 1 year earlier for half of these girls. Body mass index correlated significantly with bone mass in girls who were not anorexic (P &lt; .05, .005, and .0001 for lumbar, radius, and whole body, respectively). Bone mineral correlated significantly with body mass index in patients with anorexia nervosa as well. In addition, age at onset and duration of anorexia nervosa, but not calcium intake, activity level, or duration of amenorrhea correlated significantly with bone mineral density. It was concluded that important deficits of bone mass occur as a frequent and often early complication of anorexia nervosa in adolescence. Whole body is considerably more sensitive than midradius bone density as a measure of cortical bone loss in this illness. Low body mass index is an important predictor of this reduction in bone mass.


Author(s):  
Piotr J Czernik ◽  
Rachel M. Golonka ◽  
Saroj Chakraborty ◽  
Beng San Yeoh ◽  
Ahmed A Abokor ◽  
...  

Integration of microbiota in a host begins at birth and progresses during adolescence, forming a multidirectional system of physiologic interactions. Here, we present an instantaneous effect of natural, bacterial gut colonization on the acceleration of longitudinal and radial bone growth in germ-free born, 7-week-old male rats. Changes in bone mass and structure were analyzed after 10 days following the onset of colonization through cohousing with conventional rats and revealed unprecedented acceleration of bone accrual in cortical and trabecular compartments, increased bone tissue mineral density, improved proliferation and hypertrophy of growth plate chondrocytes, bone lengthening, and preferential deposition of periosteal bone in the tibia diaphysis. In addition, the number of small in size adipocytes increased, while the number of megakaryocytes decreased, in the bone marrow of conventionalized germ-free rats indicating that not only bone mass but also bone marrow environment is under control of gut microbiota signaling. The changes in bone status paralleled with a positive shift in microbiota composition toward short chain fatty acids (SCFA)-producing microbes and a considerable increase in cecal SCFA concentrations, specifically butyrate. Further, reconstitution of the host holobiont increased hepatic expression of IGF-1 and its circulating levels. Elevated serum levels of 25-hydroxy vitamin D and alkaline phosphatase pointed toward an active process of bone formation. The acute stimulatory effect on bone growth occurred independently of body mass increase. Overall, the presented model of conventionalized germ-free rats could be used to study microbiota-based therapeutics for combatting dysbiosis-related bone disorders.


2002 ◽  
Vol 55 (4) ◽  
pp. 219-222 ◽  
Author(s):  
Naoto SUZUKI ◽  
Akihiro DAIRAKU ◽  
Tomio KATAGAI ◽  
Gensei TSUNODA ◽  
Kazuyuki SUZUKI ◽  
...  

2008 ◽  
Vol 7 (2) ◽  
pp. 46-51
Author(s):  
O. S. Dranichnikova ◽  
V. D. Zavadovskaya ◽  
V. M. Alifirova

A number of investigations revealed a problem of osteopenic syndrome in patients with multiple sclerosis but there is no common opinion concerning factors which lead to its development. We observed 65 patients with multiple sclerosis with various type of its course and disability status of several degree based upon EDSS scale. Ultrasound osteometry of the calcaneus, computer tomography of QCT of L1—L3 vertebras were performed, serum crosslaps, N-MID osteocalcin were used. Decreased bone density, injured bone microarchitectonics and suppression of bone formation and resorption, which were correlated EDSS were found. Correlations with other factors (growth, weight, gender, and number of steroid therapy sessions ) for these parameters was not revealed. This allowed to conclude that the main reason of decreased bone mass in patients with multiple sclerosis is the dramatic decrease in physical activity.


Sign in / Sign up

Export Citation Format

Share Document