The Experts below are selected from a list of 360 Experts worldwide ranked by ideXlab platform
Ayako Shiraishi - One of the best experts on this subject based on the ideXlab platform.
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alfacalcidol inhibits bone resorption and stimulates formation in an Ovariectomized Rat model of osteoporosis distinct actions from estrogen
Journal of Bone and Mineral Research, 2010Co-Authors: Ayako Shiraishi, Noboru Kubodera, Satoshi Takeda, Toshimi Masaki, Yoshinobu Higuchi, Yasushi Uchiyama, M Kyoji D Ikeda, K. Sato, Toshitaka Nakamura, Toshio MatsumotoAbstract:Although alfacalcidol has been widely used for the treatment of osteoporosis in certain countries, its mechanism of action in bone, especially in the vitamin D–replete state, remains unclear. Here we provide histomorphometric as well as biochemical evidence that alfacalcidol suppresses osteoclastic bone resorption in an Ovariectomized Rat model of osteoporosis. Furthermore, when compared with 17β-estradiol, a representative antiresorptive drug, it is evident that alfacalcidol causes a dose-dependent suppression of bone resorption, and yet maintains or even stimulates bone formation, as reflected in increases in serum osteocalcin levels and bone formation Rate at both trabecular and cortical sites. 17β-Estradiol, which suppresses bone resorption to the same extent as alfacalcidol, causes a parallel reduction in the biochemical and histomorphometric markers of bone formation. As a final outcome, treatment with alfacalcidol increases bone mineral density and improves mechanical strength more effectively than 17β-estradiol, with a more pronounced difference in cortical bone. We conclude that estrogens depress bone turnover primarily by suppressing bone resorption and, as a consequence, bone formation as well, whereas alfacalcidol “supercouples” these processes, in that it suppresses bone resorption while maintaining or stimulating bone formation.
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alfacalcidol inhibits bone resorption and stimulates formation in an Ovariectomized Rat model of osteoporosis distinct actions from estrogen
Journal of Bone and Mineral Research, 2010Co-Authors: Ayako Shiraishi, Noboru Kubodera, Satoshi Takeda, Toshimi Masaki, Yoshinobu Higuchi, Yasushi Uchiyama, M Kyoji D Ikeda, K. Sato, Toshitaka Nakamura, Toshio MatsumotoAbstract:Although alfacalcidol has been widely used for the treatment of osteoporosis in certain countries, its mechanism of action in bone, especially in the vitamin D-replete state, remains unclear. Here we provide histomorphometric as well as biochemical evidence that alfacalcidol suppresses osteoclastic bone resorption in an Ovariectomized Rat model of osteoporosis. Furthermore, when compared with 17beta-estradiol, a representative antiresorptive drug, it is evident that alfacalcidol causes a dose-dependent suppression of bone resorption, and yet maintains or even stimulates bone formation, as reflected in increases in serum osteocalcin levels and bone formation Rate at both trabecular and cortical sites. 17beta-Estradiol, which suppresses bone resorption to the same extent as alfacalcidol, causes a parallel reduction in the biochemical and histomorphometric markers of bone formation. As a final outcome, treatment with alfacalcidol increases bone mineral density and improves mechanical strength more effectively than 17beta-estradiol, with a more pronounced difference in cortical bone. We conclude that estrogens depress bone turnover primarily by suppressing bone resorption and, as a consequence, bone formation as well, whereas alfacalcidol "supercouples" these processes, in that it suppresses bone resorption while maintaining or stimulating bone formation.
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a comparison of alfacalcidol and menatetrenone for the treatment of bone loss in an Ovariectomized Rat model of osteoporosis
Calcified Tissue International, 2002Co-Authors: Ayako Shiraishi, Toshimi Masaki, S Higashi, Motoo Saito, S Ikeda, Toshitaka NakamuraAbstract:: We conducted this study to evaluate the characteristic effects of alfacalcidol (ALF) and menatetrenone (VK) in preventing bone loss using an Ovariectomized Rat model of osteoporosis. Bilateral ovariectomy (OVX) or sham opeRation was performed on 10-month-old female Wistar Rats. OVX caused a significant decrease in the bone mass and the mechanical strength of the lumbar vertebra as well as the femur 6 months after surgery. VK treatment (30 mg/kg, food intake) required a 6-month period to prevent the bone loss induced by estrogen deficiency, whereas ALF (0.1 or 0.2 mg/kg, p.o.) increased the bone mass and the mechanical strength of the lumbar vertebra as well as the femur in a 3-month treatment period, far above the level in the sham-opeRated Rats. Neither ALF or VK caused hypercalcemia, despite administRation for as long as 6 months. By doing a micro-CT analysis of the vertebral trabecular microstructure, it was revealed that ALF treatment increased the interconnections and the plate-like structures and that VK significantly increased the trabecular number. It was also indicated that the increase in spinal strength by ALF treatment was closely associated with improvement of the microstructure, but not VK. The results of histomorphometric analysis showed that ALF caused a significant suppression of bone resorption yet maintained formation in the endocortical perimeter, and also stimulated bone formation in the periosteal perimeter, thereby causing an increase in cortical area. No marked effect of VK on histomorphometric parameters was observed, whereas VK as well as ALF maintained the material strength at femoral midshaft of the normal level, suggesting that VK affected bone quality and thereby prevented the decrease in mechanical strength of femur caused by OVX. In conclusion, it was demonstRated that the two drugs, ALF and VK, differed markedly in their potency and mechanisms for improving bone strength. These results have important implications in understanding the characteristic actions of vitamin K and active vitamin D on bone metabolism.
Toshio Matsumoto - One of the best experts on this subject based on the ideXlab platform.
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alfacalcidol inhibits bone resorption and stimulates formation in an Ovariectomized Rat model of osteoporosis distinct actions from estrogen
Journal of Bone and Mineral Research, 2010Co-Authors: Ayako Shiraishi, Noboru Kubodera, Satoshi Takeda, Toshimi Masaki, Yoshinobu Higuchi, Yasushi Uchiyama, M Kyoji D Ikeda, K. Sato, Toshitaka Nakamura, Toshio MatsumotoAbstract:Although alfacalcidol has been widely used for the treatment of osteoporosis in certain countries, its mechanism of action in bone, especially in the vitamin D–replete state, remains unclear. Here we provide histomorphometric as well as biochemical evidence that alfacalcidol suppresses osteoclastic bone resorption in an Ovariectomized Rat model of osteoporosis. Furthermore, when compared with 17β-estradiol, a representative antiresorptive drug, it is evident that alfacalcidol causes a dose-dependent suppression of bone resorption, and yet maintains or even stimulates bone formation, as reflected in increases in serum osteocalcin levels and bone formation Rate at both trabecular and cortical sites. 17β-Estradiol, which suppresses bone resorption to the same extent as alfacalcidol, causes a parallel reduction in the biochemical and histomorphometric markers of bone formation. As a final outcome, treatment with alfacalcidol increases bone mineral density and improves mechanical strength more effectively than 17β-estradiol, with a more pronounced difference in cortical bone. We conclude that estrogens depress bone turnover primarily by suppressing bone resorption and, as a consequence, bone formation as well, whereas alfacalcidol “supercouples” these processes, in that it suppresses bone resorption while maintaining or stimulating bone formation.
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alfacalcidol inhibits bone resorption and stimulates formation in an Ovariectomized Rat model of osteoporosis distinct actions from estrogen
Journal of Bone and Mineral Research, 2010Co-Authors: Ayako Shiraishi, Noboru Kubodera, Satoshi Takeda, Toshimi Masaki, Yoshinobu Higuchi, Yasushi Uchiyama, M Kyoji D Ikeda, K. Sato, Toshitaka Nakamura, Toshio MatsumotoAbstract:Although alfacalcidol has been widely used for the treatment of osteoporosis in certain countries, its mechanism of action in bone, especially in the vitamin D-replete state, remains unclear. Here we provide histomorphometric as well as biochemical evidence that alfacalcidol suppresses osteoclastic bone resorption in an Ovariectomized Rat model of osteoporosis. Furthermore, when compared with 17beta-estradiol, a representative antiresorptive drug, it is evident that alfacalcidol causes a dose-dependent suppression of bone resorption, and yet maintains or even stimulates bone formation, as reflected in increases in serum osteocalcin levels and bone formation Rate at both trabecular and cortical sites. 17beta-Estradiol, which suppresses bone resorption to the same extent as alfacalcidol, causes a parallel reduction in the biochemical and histomorphometric markers of bone formation. As a final outcome, treatment with alfacalcidol increases bone mineral density and improves mechanical strength more effectively than 17beta-estradiol, with a more pronounced difference in cortical bone. We conclude that estrogens depress bone turnover primarily by suppressing bone resorption and, as a consequence, bone formation as well, whereas alfacalcidol "supercouples" these processes, in that it suppresses bone resorption while maintaining or stimulating bone formation.
Toshitaka Nakamura - One of the best experts on this subject based on the ideXlab platform.
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alfacalcidol inhibits bone resorption and stimulates formation in an Ovariectomized Rat model of osteoporosis distinct actions from estrogen
Journal of Bone and Mineral Research, 2010Co-Authors: Ayako Shiraishi, Noboru Kubodera, Satoshi Takeda, Toshimi Masaki, Yoshinobu Higuchi, Yasushi Uchiyama, M Kyoji D Ikeda, K. Sato, Toshitaka Nakamura, Toshio MatsumotoAbstract:Although alfacalcidol has been widely used for the treatment of osteoporosis in certain countries, its mechanism of action in bone, especially in the vitamin D–replete state, remains unclear. Here we provide histomorphometric as well as biochemical evidence that alfacalcidol suppresses osteoclastic bone resorption in an Ovariectomized Rat model of osteoporosis. Furthermore, when compared with 17β-estradiol, a representative antiresorptive drug, it is evident that alfacalcidol causes a dose-dependent suppression of bone resorption, and yet maintains or even stimulates bone formation, as reflected in increases in serum osteocalcin levels and bone formation Rate at both trabecular and cortical sites. 17β-Estradiol, which suppresses bone resorption to the same extent as alfacalcidol, causes a parallel reduction in the biochemical and histomorphometric markers of bone formation. As a final outcome, treatment with alfacalcidol increases bone mineral density and improves mechanical strength more effectively than 17β-estradiol, with a more pronounced difference in cortical bone. We conclude that estrogens depress bone turnover primarily by suppressing bone resorption and, as a consequence, bone formation as well, whereas alfacalcidol “supercouples” these processes, in that it suppresses bone resorption while maintaining or stimulating bone formation.
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alfacalcidol inhibits bone resorption and stimulates formation in an Ovariectomized Rat model of osteoporosis distinct actions from estrogen
Journal of Bone and Mineral Research, 2010Co-Authors: Ayako Shiraishi, Noboru Kubodera, Satoshi Takeda, Toshimi Masaki, Yoshinobu Higuchi, Yasushi Uchiyama, M Kyoji D Ikeda, K. Sato, Toshitaka Nakamura, Toshio MatsumotoAbstract:Although alfacalcidol has been widely used for the treatment of osteoporosis in certain countries, its mechanism of action in bone, especially in the vitamin D-replete state, remains unclear. Here we provide histomorphometric as well as biochemical evidence that alfacalcidol suppresses osteoclastic bone resorption in an Ovariectomized Rat model of osteoporosis. Furthermore, when compared with 17beta-estradiol, a representative antiresorptive drug, it is evident that alfacalcidol causes a dose-dependent suppression of bone resorption, and yet maintains or even stimulates bone formation, as reflected in increases in serum osteocalcin levels and bone formation Rate at both trabecular and cortical sites. 17beta-Estradiol, which suppresses bone resorption to the same extent as alfacalcidol, causes a parallel reduction in the biochemical and histomorphometric markers of bone formation. As a final outcome, treatment with alfacalcidol increases bone mineral density and improves mechanical strength more effectively than 17beta-estradiol, with a more pronounced difference in cortical bone. We conclude that estrogens depress bone turnover primarily by suppressing bone resorption and, as a consequence, bone formation as well, whereas alfacalcidol "supercouples" these processes, in that it suppresses bone resorption while maintaining or stimulating bone formation.
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a comparison of alfacalcidol and menatetrenone for the treatment of bone loss in an Ovariectomized Rat model of osteoporosis
Calcified Tissue International, 2002Co-Authors: Ayako Shiraishi, Toshimi Masaki, S Higashi, Motoo Saito, S Ikeda, Toshitaka NakamuraAbstract:: We conducted this study to evaluate the characteristic effects of alfacalcidol (ALF) and menatetrenone (VK) in preventing bone loss using an Ovariectomized Rat model of osteoporosis. Bilateral ovariectomy (OVX) or sham opeRation was performed on 10-month-old female Wistar Rats. OVX caused a significant decrease in the bone mass and the mechanical strength of the lumbar vertebra as well as the femur 6 months after surgery. VK treatment (30 mg/kg, food intake) required a 6-month period to prevent the bone loss induced by estrogen deficiency, whereas ALF (0.1 or 0.2 mg/kg, p.o.) increased the bone mass and the mechanical strength of the lumbar vertebra as well as the femur in a 3-month treatment period, far above the level in the sham-opeRated Rats. Neither ALF or VK caused hypercalcemia, despite administRation for as long as 6 months. By doing a micro-CT analysis of the vertebral trabecular microstructure, it was revealed that ALF treatment increased the interconnections and the plate-like structures and that VK significantly increased the trabecular number. It was also indicated that the increase in spinal strength by ALF treatment was closely associated with improvement of the microstructure, but not VK. The results of histomorphometric analysis showed that ALF caused a significant suppression of bone resorption yet maintained formation in the endocortical perimeter, and also stimulated bone formation in the periosteal perimeter, thereby causing an increase in cortical area. No marked effect of VK on histomorphometric parameters was observed, whereas VK as well as ALF maintained the material strength at femoral midshaft of the normal level, suggesting that VK affected bone quality and thereby prevented the decrease in mechanical strength of femur caused by OVX. In conclusion, it was demonstRated that the two drugs, ALF and VK, differed markedly in their potency and mechanisms for improving bone strength. These results have important implications in understanding the characteristic actions of vitamin K and active vitamin D on bone metabolism.
John F Aloia - One of the best experts on this subject based on the ideXlab platform.
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additive effect of treadmill exercise and 17β estradiol replacement on prevention of tibial bone loss in adult Ovariectomized Rat
Journal of Bone and Mineral Research, 2009Co-Authors: James K Yeh, Chung C Liu, John F AloiaAbstract:The effects of 17 beta-estradiol (E2) and treadmill exercise on tibial bone mass, tibial uptake of 45Ca, and proximal tibia osteoblast and osteoclast cell number were determined in adult Ovariectomized Rats. Female Rats aged 10 months were Ovariectomized and divided into five groups: (1) sham-opeRated; (2) Ovariectomized; (3) Ovariectomized, given 10 micrograms E2 biweekly; (4) Ovariectomized, trained to exercise on a treadmill daily; and (5) Ovariectomized, given E2 and exercised. E2 and/or exercise interventions were started 2 months following surgery and continued for 4 months. The calcium content of the tibial metaphysis and diaphysis and the proximal cancellous bone (BV/TV) were lower in the Ovariectomized than in the sham-opeRated controls 6 months after ovariectomy. This lower bone content was associated with a greater bone uptake of 45Ca and a greater number of osteoblasts and osteoclasts in the proximal tibia compared to the control Rats. The metaphyseal calcium content was higher and the 45Ca uptake and osteoblast and osteoclast number were lower in the E2-treated Rats than in the nontreated Rats. In the exercised group, higher diaphyseal calcium content and proximal cancellous bone were associated with lower bone resorption parameters without a significant effect on bone formation. This study demonstRates that E2 primarily influences tibial cancellous bone of the Ovariectomized Rat and a positive adaptation to exercise occurs in both cancellous and cortical bone. Under estrogen deficiency, E2 replacement suppresses increased bone formation and resorption; exercise suppresses mainly bone resorption. The effects of E2 replacement and exercise training are independent and additive.
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effects of estrogen and growth hormone on skeleton in the Ovariectomized Rat with hypophysectomy
American Journal of Physiology-endocrinology and Metabolism, 1997Co-Authors: James K Yeh, John F Aloia, Mengmeng ChenAbstract:To investigate whether growth hormone (GH) and 17β-estradiol (E2) replacement can prevent osteopenia induced by pituitary and ovarian hormone deficiency [by hypophysectomy and ovariectomy (HX+OV)],...
Toshimi Masaki - One of the best experts on this subject based on the ideXlab platform.
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alfacalcidol inhibits bone resorption and stimulates formation in an Ovariectomized Rat model of osteoporosis distinct actions from estrogen
Journal of Bone and Mineral Research, 2010Co-Authors: Ayako Shiraishi, Noboru Kubodera, Satoshi Takeda, Toshimi Masaki, Yoshinobu Higuchi, Yasushi Uchiyama, M Kyoji D Ikeda, K. Sato, Toshitaka Nakamura, Toshio MatsumotoAbstract:Although alfacalcidol has been widely used for the treatment of osteoporosis in certain countries, its mechanism of action in bone, especially in the vitamin D–replete state, remains unclear. Here we provide histomorphometric as well as biochemical evidence that alfacalcidol suppresses osteoclastic bone resorption in an Ovariectomized Rat model of osteoporosis. Furthermore, when compared with 17β-estradiol, a representative antiresorptive drug, it is evident that alfacalcidol causes a dose-dependent suppression of bone resorption, and yet maintains or even stimulates bone formation, as reflected in increases in serum osteocalcin levels and bone formation Rate at both trabecular and cortical sites. 17β-Estradiol, which suppresses bone resorption to the same extent as alfacalcidol, causes a parallel reduction in the biochemical and histomorphometric markers of bone formation. As a final outcome, treatment with alfacalcidol increases bone mineral density and improves mechanical strength more effectively than 17β-estradiol, with a more pronounced difference in cortical bone. We conclude that estrogens depress bone turnover primarily by suppressing bone resorption and, as a consequence, bone formation as well, whereas alfacalcidol “supercouples” these processes, in that it suppresses bone resorption while maintaining or stimulating bone formation.
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alfacalcidol inhibits bone resorption and stimulates formation in an Ovariectomized Rat model of osteoporosis distinct actions from estrogen
Journal of Bone and Mineral Research, 2010Co-Authors: Ayako Shiraishi, Noboru Kubodera, Satoshi Takeda, Toshimi Masaki, Yoshinobu Higuchi, Yasushi Uchiyama, M Kyoji D Ikeda, K. Sato, Toshitaka Nakamura, Toshio MatsumotoAbstract:Although alfacalcidol has been widely used for the treatment of osteoporosis in certain countries, its mechanism of action in bone, especially in the vitamin D-replete state, remains unclear. Here we provide histomorphometric as well as biochemical evidence that alfacalcidol suppresses osteoclastic bone resorption in an Ovariectomized Rat model of osteoporosis. Furthermore, when compared with 17beta-estradiol, a representative antiresorptive drug, it is evident that alfacalcidol causes a dose-dependent suppression of bone resorption, and yet maintains or even stimulates bone formation, as reflected in increases in serum osteocalcin levels and bone formation Rate at both trabecular and cortical sites. 17beta-Estradiol, which suppresses bone resorption to the same extent as alfacalcidol, causes a parallel reduction in the biochemical and histomorphometric markers of bone formation. As a final outcome, treatment with alfacalcidol increases bone mineral density and improves mechanical strength more effectively than 17beta-estradiol, with a more pronounced difference in cortical bone. We conclude that estrogens depress bone turnover primarily by suppressing bone resorption and, as a consequence, bone formation as well, whereas alfacalcidol "supercouples" these processes, in that it suppresses bone resorption while maintaining or stimulating bone formation.
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a comparison of alfacalcidol and menatetrenone for the treatment of bone loss in an Ovariectomized Rat model of osteoporosis
Calcified Tissue International, 2002Co-Authors: Ayako Shiraishi, Toshimi Masaki, S Higashi, Motoo Saito, S Ikeda, Toshitaka NakamuraAbstract:: We conducted this study to evaluate the characteristic effects of alfacalcidol (ALF) and menatetrenone (VK) in preventing bone loss using an Ovariectomized Rat model of osteoporosis. Bilateral ovariectomy (OVX) or sham opeRation was performed on 10-month-old female Wistar Rats. OVX caused a significant decrease in the bone mass and the mechanical strength of the lumbar vertebra as well as the femur 6 months after surgery. VK treatment (30 mg/kg, food intake) required a 6-month period to prevent the bone loss induced by estrogen deficiency, whereas ALF (0.1 or 0.2 mg/kg, p.o.) increased the bone mass and the mechanical strength of the lumbar vertebra as well as the femur in a 3-month treatment period, far above the level in the sham-opeRated Rats. Neither ALF or VK caused hypercalcemia, despite administRation for as long as 6 months. By doing a micro-CT analysis of the vertebral trabecular microstructure, it was revealed that ALF treatment increased the interconnections and the plate-like structures and that VK significantly increased the trabecular number. It was also indicated that the increase in spinal strength by ALF treatment was closely associated with improvement of the microstructure, but not VK. The results of histomorphometric analysis showed that ALF caused a significant suppression of bone resorption yet maintained formation in the endocortical perimeter, and also stimulated bone formation in the periosteal perimeter, thereby causing an increase in cortical area. No marked effect of VK on histomorphometric parameters was observed, whereas VK as well as ALF maintained the material strength at femoral midshaft of the normal level, suggesting that VK affected bone quality and thereby prevented the decrease in mechanical strength of femur caused by OVX. In conclusion, it was demonstRated that the two drugs, ALF and VK, differed markedly in their potency and mechanisms for improving bone strength. These results have important implications in understanding the characteristic actions of vitamin K and active vitamin D on bone metabolism.