Biomedical subjects

J U Lindgren

Publications and source records attributed to J U Lindgren.

44 records · Page 3Linked to original sources

PubMed1984

Effects of 1 alpha OHD2 on bone tissue. Studies of 1 alpha OHD2 and 1 alpha OHD3 in normal rats and in rats treated with prednisolone.

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 micrograms 1 alpha OHD2 or 0.5 micrograms 1 alpha OHD3 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 1 alpha OHD3 had an increased serum calcium concentration even when simultaneously treated with prednisolone. 1 alpha OHD2 did not cause hypercalcaemia. The decrease in bone density caused by prednisolone was prevented by the administration of 1 alpha OHD2. Rats receiving 1 alpha OHD3 together with prednisolone still exhibited a lower bone density. Furthermore, 1 alpha OHD3 decreased bone mass in normal rats and caused a higher mean value of osteoclasts/area whereas 1 alpha OHD2 reduced the number of osteoclasts/area. The study indicates that 1 alpha OHD2 is an effective vitamin D analogue with a lower tendency to cause bone resorption.

Animals↗

PubMed1984

Osteoporosis. Experimental and clinical studies.

Combined experimental and clinical research illustrates not only the multiplicity of questions for research on osteoporosis but also the difficulty of penetrating such a complicated clinical problem as treatment and prevention of osteoporosis. Without thorough knowledge of the pathomechanisms responsible for the development of the condition and a rational working hypothesis, any attempt to develop a new approach seems unlikely to succeed.

Administration, Oral↗

PubMed1983

Oral 1,25(OH)2D3: an effective prophylactic treatment for glucocorticoid osteopenia in rats.

Eighty-eight adult male Sprague-Dawley rats were given a diet with either (a) 0.5% Ca and 0.6% P or (b) 0.01% Ca and 0.6% P. Osteopenia was created by adding prednisolone to the diet. The prophylactic effect of oral 1,25(OH)2D3 on the osteopenia was studied. It was found that prednisolone osteopenia in the rat was associated with defective Ca absorption. By giving an oral dose of 1,25(OH)2D3, it was possible to maintain normal Ca absorption during prednisolone treatment and to prevent the bone loss. No significant hypercalcemia or any kidney calcifications were seen. These results are in contrast to earlier findings, in which subcutaneous administration of 1,25(OH)2D3 failed to prevent prednisolone osteopenia because of its tendency to increase bone resorption.

Animals↗

PubMed1983

Studies of bone tissue in rats treated by prednisolone and 1,25-(OH)2D3.

Adult male rats were treated for six weeks by prednisolone and/or 1,25-(OH)2D3 and given a diet containing either 0.5% calcium or 0.01% Ca and 0.6% phosphorus. Both prednisolone administration and a low-Ca diet were associated with a lower bone mass than that observed in control rats given a 0.5% Ca diet. The percentage of osteoid surface was decreased in rats given prednisolone; these rats also had a lower osteoclast number. The results were consistent with a lower bone turnover during prednisolone treatment. Administration of 1,25-(OH)2D3, resulting in a slightly higher mean level of 1,25-(OH)2D3 in serum, had a positive effect on bone mass, which may be related to increased osteoblastic activity; no increase in the osteoclast number occurred.

Animals↗

PubMed1982

Effect of 1,25-dihydroxyvitamin D3 on osteopenia induced by prednisolone in adult rats.

Adult male rats were fed a diet containing 0.15% calcium, 0.3% phosphorus, an either 100, 50, or 20 mg of prednisolone per kg of diet. All these levels of prednisolone led to osteopenia, decreased intestinal absorption of calcium, slightly lower serum calcium and phosphorus, and a decreased level of serum 1,25-dihydroxyvitamin D3. Exogenous parenteral 1,25-dihydroxyvitamin D3 corrected steroid-induced changes in serum calcium and phosphorus, but could not completely correct the low intestinal calcium transport; nor did it prevent the development of osteopenia. The prednisolone-induced osteopenia seems at least in part to be caused by impaired intestinal calcium transport. The impaired calcium transport may be the result of low levels of 1,25-dihydroxyvitamin D3 and a direct effect of presnisolone on the intestine.

Animals↗

PubMed1981

Effects of 1,24 dihydroxyvitamin D3 and calcitonin on fracture healing in adult rats.

Calcitonin and 1.25(OH)2D3 have opposite effects on the serum concentrations of Ca and P, as well as on bone resorption, and can be observed in the process of healing of standardized fracture in adult rats. The rats given 1.25(OH)2D3 had a stronger fracture callus and slightly less pronounced postfracture osteopenia. Calcitonin did not significantly influence the fracture healing but had a pronounced effect in preventing the osteopenia. The effects of 1.25(OH)2D3 are believed to be indirect, i.e., through the changes in the serum Ca X P product, whereas the osteopenia preventing action of calcitonin may come from direct effect on bone.

Animals↗

PubMed1979

Effect of 1-alpha-hydroxyvitamin D3 on osteoporosis in rats induced by oophorectomy.

Fifty adult female rats were used to study the effect of 1-alpha-hydroxyvitamin D3 (1alpha-OH-D3) on bone after oophorectomy. The experimental period was 6 months. At the end of the experiment the femurs and the tibias were investigated for bone mass and composition. Significant signs of osteopenia occurred as a result of oophorectomy. The treatment with 1alpha-OH-D3 induced only minor changes in blood chemistry but increased bone mass significantly. The findings support the view that 1alpha-OH-D3 may be a valuable tool in the treatment of osteoporosis resulting from ovarian insufficiency.

Animals↗

PubMed1976

Studies of the calcium accretion rate of bone during immobilization in intact and thyroparathyroidectomized adult rats.

In order to study the role played by the thyroid and the parathyroid glands in the development of osteoporosis induced by immobilization, 153 male adult Sprague-Dawley rats allocated in two groups were used. The animals of one group were thyroparathyroidectomized; those of the other group were left intact. Each group was then divided into two subgroups; in one the right hind leg of the animals were immobilized by an elastic adhesive bandage. The animals were observed for varying periods of time up to 16 weeks. Studies of bone mass and 45Ca accretion rate of the right and left femur and tibia were performed in all animals. The results indicate that disuse osteoporosis occurs in rats in the virtual absence of the thyroid and parathyroid glands. The bone loss of the immobilized femur and tibia was less pronounced in thyroparathyroidectomized rats compared to intact rats. The uptake of 45Ca in bone treated by immobilization as compared to the non-immobilized bone was found to be increased to the same proportion in thyroparathyroidectomized and in intact rats. The calcium-accretion rate of non-immobilized bone was lower in thyroparathyroidectomized than in intact rats. The observations indicate that in the rat the parathyroid and thyroid hormones influence the rate of bone turnover and thereby the rate of development of disuse osteoporosis.

Animals↗