scholarly journals Treatment with the combination of ibandronate plus eldecalcitol has a synergistic effect on inhibition of bone resorption without suppressing bone formation in ovariectomized rats

Bone ◽  
2015 ◽  
Vol 81 ◽  
pp. 449-458 ◽  
Author(s):  
Sadaoki Sakai ◽  
Satoshi Takeda ◽  
Masanori Sugimoto ◽  
Masaru Shimizu ◽  
Yasushi Shimonaka ◽  
...  
2004 ◽  
Vol 19 (7) ◽  
pp. 1144-1153 ◽  
Author(s):  
Sophie Schaller ◽  
Kim Henriksen ◽  
Christina Sveigaard ◽  
Anne-Marie Heegaard ◽  
Nathalie Hélix ◽  
...  

1994 ◽  
Vol 267 (6) ◽  
pp. E853-E859 ◽  
Author(s):  
J. H. Tobias ◽  
A. Gallagher ◽  
T. J. Chambers

Although androgens are thought to be important for skeletal maintenance in females and males, little is known about the mechanisms involved. To investigate this question further, we examined the effects of administering 0.01, 0.1, or 1.0 mg/kg 5 alpha-dihydrotestosterone (DHT) for 60 days on the skeleton of ovariectomized rats. Treatment was delayed until 90 days after ovariectomy to enable bone loss to stabilize. We found that ovariectomy markedly reduced cancellous bone volume of the proximal tibial metaphysis due to a combination of loss and thinning of trabeculae. Cancellous bone volume was partially restored by all doses of DHT, with trabecular thickness, but not number, returning to that of sham-operated animals. DHT also stimulated longitudinal bone growth and endosteal and periosteal bone formation and suppressed histomorphometric indexes of cancellous bone resorption. This suggests that DHT influences skeletal metabolism in osteopenic ovariectomized rats both by stimulating bone formation and suppressing resorption, although it is unclear which, if any, of these actions predominate at cancellous sites.


1994 ◽  
Vol 142 (1) ◽  
pp. 61-67 ◽  
Author(s):  
J H Tobias ◽  
A Gallagher ◽  
T J Chambers

Abstract Although short-term administration of oestradiol-17β (OE2) stimulates cancellous bone formation in the rat, this is replaced by a tendency to suppression after prolonged treatment. Hence, in rats rendered osteopaenic by ovariectomy, OE2 administration fails either to induce a sustained increase in bone formation or to restore bone volume. A possible explanation for this failure is that OE2 also inhibits bone resorption, secondarily suppressing bone formation through coupling mechanisms. We therefore investigated whether the effects of OE2 treatment might be modified by intermittently stimulating bone resorption with retinoic acid (120mg/kg daily) for 4 out of every 20 days. We found, in a preliminary experiment using intact animals, that intermittent retinoic acid reduced cancellous bone volume, consistent with previously documented stimulation of bone resorption by retinoic acid. Rats were then rendered osteopaenic by ovariectomy, and given vehicle, retinoic acid and/or OE2. We found that animals treated with intermittent retinoic acid and OE2 showed a substantial increase in cancellous bone volume compared with ovariectomized animals treated with vehicle, retinoic acid alone or OE2 alone. Therefore, intermittent retinoic acid appears to cause a net increase in bone formation over resorption when given to ovariectomized animals in conjunction with OE2. We conclude that the effects of OE2 on cancellous bone are modified by intermittent treatment with retinoic acid, resulting in a substantial increase in bone volume. Journal of Endocrinology (1994) 142, 61–67


2006 ◽  
Vol 84 (10) ◽  
pp. 993-1002 ◽  
Author(s):  
Supaporn Puntheeranurak ◽  
Narattaphol Charoenphandhu ◽  
Nateetip Krishnamra

Although an increase in trabecular-bone calcium deposition has been shown to be regulated by prolactin during lactation, the physiological significance of prolactin in bone calcium metabolism in nonlactating rats remains unclear. This investigation sought to demonstrate the effects of endogenous prolactin and a high physiological dose of exogenous prolactin on bone turnover and bone calcium deposition in normal female rats, using the 45Ca-labeling technique. Our results showed that suppression of endogenous prolactin with 6 mg/kg bromocriptine for 15 days significantly enhanced bone formation, but not bone resorption, in primarily trabecular sites, resulting in a significant increase in calcium deposition in the sternum and vertebrae, from –0.20 ± 0.07 to 0.40 ± 0.09 (p < 0.05) and –0.07 ± 0.11 to 0.34 ± 0.06 (p < 0.05) mmol Ca·(g dry mass)–1, respectively. Similarly, 2.5 mg/kg prolactin, a high physiological dose, increased sternal and vertebral calcium deposition, from –0.20 ± 0.07 to 0.24 ± 0.09 (p < 0.05) and –0.07 ± 0.11 to 0.25 ± 0.18 (p < 0.05) mmol Ca·(g dry mass)–1, respectively, by increasing bone formation more than bone resorption. However, as expected, prolactin had no effect on the tibia or femur, which are primarily cortical sites. Because several actions of prolactin have been known to be estradiol-dependent, we further investigated the dependence of prolactin action on 17β-estradiol. We found that 2.5 mg/kg prolactin did not increase sternal calcium deposition in ovariectomized rats. However, 10 µg/kg 17β-estradiol supplementation restored the action of prolactin. Ovariectomized rats given 17β-estradiol plus prolactin also manifested slightly but significantly higher sternal total calcium content than sham-operated rats, (4.58 ± 0.12 vs. 4.36 ± 0.11 mmol Ca·(g dry mass)–1 (p < 0.05)). We concluded that a high physiological dose of prolactin promoted calcium deposition in primarily trabecular sites of nonlactating rats. This effect was diminished after ovariectomy. In addition, we showed that basal endogenous prolactin played a role in the maintenance of normal trabecular-bone turnover.


2013 ◽  
Vol 2013 ◽  
pp. 1-9 ◽  
Author(s):  
Rafaela G. Feresin ◽  
Sarah A. Johnson ◽  
Marcus L. Elam ◽  
Jeong-Su Kim ◽  
Dania A. Khalil ◽  
...  

The present study examined the dose-dependent effect of vitamin E in reversing bone loss in ovariectomized (Ovx) rats. Sprague-Dawley rats were either Sham-operated (Sham) or Ovx and fed control diet for 120 days to lose bone. Subsequently, rats were divided into 5 groups (n=12/group): Sham, Ovx-control, low dose (Ovx + 300 mg/kg diet; LD), medium dose (Ovx + 525 mg/kg diet; MD), and high dose (Ovx + 750 mg/kg diet; HD) of vitamin E and sacrificed after 100 days. Animals receiving MD and HD of vitamin E had increased serum alkaline phosphatase compared to the Ovx-control group. Bone histomorphometry analysis indicated a decrease in bone resorption as well as increased bone formation and mineralization in the Ovx groups supplemented with MD and HD of vitamin E. Microcomputed tomography findings indicated no effects of vitamin E on trabecular bone of fifth lumbar vertebrae. Animals receiving HD of vitamin E had enhanced fourth lumbar vertebra quality as evidenced by improved ultimate and yield load and stress when compared to Ovx-control group. These findings demonstrate that vitamin E improves bone quality, attenuates bone resorption, and enhances the rate of bone formation while being unable to restore bone density and trabecular bone structure.


2018 ◽  
Vol 36 (1) ◽  
pp. 1
Author(s):  
Hartiningsih Hartiningsih ◽  
Devita Anggraeni

Calcitriol supplementation in ovariectomized rats decreased bone resorption and increased bone formation, however, it depend on dose. The objective of the research was to study the response of femur bone in osteoporosis rats consuming calcitriol. Thirty female Wistar rats at 8 weeks of age were randomly divided into six groups (sham operated rats as normal control rats/group N and NK, ovariectomized control rats/group Ov and OvK, ovariectomized rats/group OvDand OvE) of five each. All rats were fed standard diet for 8 weeks. At 16 weeks  of age, group N and Ov  were euthanized, the right femur were taken for histopathological  examination. Group NK and OvK were fed a standard diet, group OvD was fed a standard diet +40ng calcitriol;  and group OvE was fed a standard diet+25µg ethynil ethyl estradiol. Treatments were done for six weeks. At the end of study, blood samples were taken from plexus orbitalis medialis for estrogen analysis. All rats were euthanized using ketamine10% and xylazine 2%. Right femur was taken for histopathological examination  using hematoxylin and eosin stain, and immunohistochemistry using monoclonal antibody anti TRAP5b which was detected with streptavidin-biotin.         The results showed that estradiol level of the rats in group OvD was not significantly different compared with the rats in OvK group, however, it was significanly lower compared to the rats in group OvE. Histopathologic figure of right distal femur metaphysis in group OvD was shown lesser adipocyte in the bone marrow and more trabecular bone speculum compared to group  OvK, however, there was more adipocyte in the bone marrow and lesser trabecular bone speculum compared to group OvE. Immunohistochemistry of distal femur metaphysis in group OvD and OvE were revealed tartrate resistant alkaline phosphatase 5b (TRAP5b) expression in trabecular bone, which was located in bone marrow space and trabecular speculum surface as well. Based on the results, it can be concluded that calcitriol 40ng/day supplementation in osteoporosis rats for 6 weeks decreased bone resorption and increased bone formation distal femur metaphysis.


Bone ◽  
2000 ◽  
Vol 26 (1) ◽  
pp. 43-53 ◽  
Author(s):  
T Tanizawa ◽  
A Yamaguchi ◽  
Y Uchiyama ◽  
C Miyaura ◽  
T Ikeda ◽  
...  

Nutrients ◽  
2020 ◽  
Vol 12 (10) ◽  
pp. 3210
Author(s):  
Farida S. Nirmala ◽  
Hyunjung Lee ◽  
Ji-Sun Kim ◽  
Taeyoul Ha ◽  
Chang Hwa Jung ◽  
...  

Although drug therapies are available for postmenopausal osteoporosis, these drugs are not free of side effects and long-term adherence to them are low. A safe and effective nutritional approach to counter postmenopausal osteoporosis is an important research goal. We fed ovariectomized (OVX) Sprague–Dawley rats a diet supplemented with 1% or 2% green tomato extract (GTE). After 12 weeks, micro-computed tomography scans revealed that GTE supplementation effectively prevented distal femur bone loss. This prevention was due to improved bone formation and suppressed bone resorption as observed by the regulation of osteoblast and osteoclast activities. GTE supplementation also improved bone formation through Bmp2-Smad 1/5/8-Runx2 signaling, while bone resorption was regulated by the receptor activator of nuclear factor kappa-B (RANKL)/osteoprogeterin (OPG) pathway. These results suggest that GTE supplementation prevents severe postmenopausal bone loss by maintaining the regulation of bone homeostasis in OVX rats. GTE as a diet supplement might be a potential novel alternative for the prevention of postmenopausal osteoporosis.


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