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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, Toshitaka Nakamura, K. Sato, 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, Toshitaka Nakamura, K. Sato, 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.
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, Toshitaka Nakamura, K. Sato, 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, Toshitaka Nakamura, K. Sato, 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.
Stefan R Bornstein - One of the best experts on this subject based on the ideXlab platform.
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impact of aldosterone synthase inhibitor fad286 on steroid hormone profile in human adrenocortical cells
Hormone and Metabolic Research, 2017Co-Authors: Coy Brunssen, Anja Hofmann, Mirko Peitzsch, Annika Frenzel, Nicholas F. Brown, Steven M. Weldon, Christian G Ziegler, Graeme Eisenhofer, H S Willenberg, Stefan R BornsteinAbstract:Inhibition of aldosterone synthase (CYP11B2) is an alternative treatment option to mineralocorticoid receptor antagonism to prevent harmful aldosterone effects. FAD286 is the best characterized aldosterone synthase inhibitor. However, to date, no study has used sensitive liquid chromatography-tandem mass spectrometry to characterize in detail the effect of FAD286 on the secreted steroid hormone profile of adrenocortical cells. Basal aldosterone production in NCI-H295R cells was detectable and 9-fold elevated after stimulation with angiotensin II. FAD286 inhibited this increase, showing a maximal effect at 10 nmol/l. Higher concentrations of FAD286 did not further reduce aldosterone concentrations, but showed a Parallel Reduction in corticosterone, cortisol and cortisone levels, reflecting additional inhibition of steroid-11β-hydroxylase (CYP11B1). Pregnenolone, progesterone and 17-OH-progesterone levels remained unaffected. In conclusion, the aldosterone synthase inhibitor FAD286 lowers angiotensin II-induced aldosterone concentrations in adrenocortical cells but the relative lack of selectivity over CYP11B1 is evident at higher FAD286 concentrations.
Satoshi Takeda - 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, Toshitaka Nakamura, K. Sato, 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, Toshitaka Nakamura, K. Sato, 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, Toshitaka Nakamura, K. Sato, 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, Toshitaka Nakamura, K. Sato, 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.
