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Niklas Andersson Center for Bone Research at the Sahlgrenska Academy, Division of Endocrinology, Department of Internal Medicine, Göteborg University, Gröna stråket 8 SE-413 45 Göteborg, Sweden
Department of Rheumatology and Inflammation Research at the Sahlgrenska Academy, Göteborg University, Guldhedsgatan 10, SE-413 46 Göteborg, Sweden
Department of Physiology, Göteborg University, Medicinaregatan 9, Box 434 SE-405 30 Göteborg, Sweden
Department of Pharmacology, Göteborg University, Medicinaregatan 9, Box 434 SE-405 30 Göteborg, Sweden

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Ulrika Islander Center for Bone Research at the Sahlgrenska Academy, Division of Endocrinology, Department of Internal Medicine, Göteborg University, Gröna stråket 8 SE-413 45 Göteborg, Sweden
Department of Rheumatology and Inflammation Research at the Sahlgrenska Academy, Göteborg University, Guldhedsgatan 10, SE-413 46 Göteborg, Sweden
Department of Physiology, Göteborg University, Medicinaregatan 9, Box 434 SE-405 30 Göteborg, Sweden
Department of Pharmacology, Göteborg University, Medicinaregatan 9, Box 434 SE-405 30 Göteborg, Sweden

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Emil Egecioglu Center for Bone Research at the Sahlgrenska Academy, Division of Endocrinology, Department of Internal Medicine, Göteborg University, Gröna stråket 8 SE-413 45 Göteborg, Sweden
Department of Rheumatology and Inflammation Research at the Sahlgrenska Academy, Göteborg University, Guldhedsgatan 10, SE-413 46 Göteborg, Sweden
Department of Physiology, Göteborg University, Medicinaregatan 9, Box 434 SE-405 30 Göteborg, Sweden
Department of Pharmacology, Göteborg University, Medicinaregatan 9, Box 434 SE-405 30 Göteborg, Sweden

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Elin Löf Center for Bone Research at the Sahlgrenska Academy, Division of Endocrinology, Department of Internal Medicine, Göteborg University, Gröna stråket 8 SE-413 45 Göteborg, Sweden
Department of Rheumatology and Inflammation Research at the Sahlgrenska Academy, Göteborg University, Guldhedsgatan 10, SE-413 46 Göteborg, Sweden
Department of Physiology, Göteborg University, Medicinaregatan 9, Box 434 SE-405 30 Göteborg, Sweden
Department of Pharmacology, Göteborg University, Medicinaregatan 9, Box 434 SE-405 30 Göteborg, Sweden

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Charlotte Swanson Center for Bone Research at the Sahlgrenska Academy, Division of Endocrinology, Department of Internal Medicine, Göteborg University, Gröna stråket 8 SE-413 45 Göteborg, Sweden
Department of Rheumatology and Inflammation Research at the Sahlgrenska Academy, Göteborg University, Guldhedsgatan 10, SE-413 46 Göteborg, Sweden
Department of Physiology, Göteborg University, Medicinaregatan 9, Box 434 SE-405 30 Göteborg, Sweden
Department of Pharmacology, Göteborg University, Medicinaregatan 9, Box 434 SE-405 30 Göteborg, Sweden

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Sofia Movérare-Skrtic Center for Bone Research at the Sahlgrenska Academy, Division of Endocrinology, Department of Internal Medicine, Göteborg University, Gröna stråket 8 SE-413 45 Göteborg, Sweden
Department of Rheumatology and Inflammation Research at the Sahlgrenska Academy, Göteborg University, Guldhedsgatan 10, SE-413 46 Göteborg, Sweden
Department of Physiology, Göteborg University, Medicinaregatan 9, Box 434 SE-405 30 Göteborg, Sweden
Department of Pharmacology, Göteborg University, Medicinaregatan 9, Box 434 SE-405 30 Göteborg, Sweden

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Klara Sjögren Center for Bone Research at the Sahlgrenska Academy, Division of Endocrinology, Department of Internal Medicine, Göteborg University, Gröna stråket 8 SE-413 45 Göteborg, Sweden
Department of Rheumatology and Inflammation Research at the Sahlgrenska Academy, Göteborg University, Guldhedsgatan 10, SE-413 46 Göteborg, Sweden
Department of Physiology, Göteborg University, Medicinaregatan 9, Box 434 SE-405 30 Göteborg, Sweden
Department of Pharmacology, Göteborg University, Medicinaregatan 9, Box 434 SE-405 30 Göteborg, Sweden

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Marie K Lindberg Center for Bone Research at the Sahlgrenska Academy, Division of Endocrinology, Department of Internal Medicine, Göteborg University, Gröna stråket 8 SE-413 45 Göteborg, Sweden
Department of Rheumatology and Inflammation Research at the Sahlgrenska Academy, Göteborg University, Guldhedsgatan 10, SE-413 46 Göteborg, Sweden
Department of Physiology, Göteborg University, Medicinaregatan 9, Box 434 SE-405 30 Göteborg, Sweden
Department of Pharmacology, Göteborg University, Medicinaregatan 9, Box 434 SE-405 30 Göteborg, Sweden

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Hans Carlsten Center for Bone Research at the Sahlgrenska Academy, Division of Endocrinology, Department of Internal Medicine, Göteborg University, Gröna stråket 8 SE-413 45 Göteborg, Sweden
Department of Rheumatology and Inflammation Research at the Sahlgrenska Academy, Göteborg University, Guldhedsgatan 10, SE-413 46 Göteborg, Sweden
Department of Physiology, Göteborg University, Medicinaregatan 9, Box 434 SE-405 30 Göteborg, Sweden
Department of Pharmacology, Göteborg University, Medicinaregatan 9, Box 434 SE-405 30 Göteborg, Sweden

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Claes Ohlsson Center for Bone Research at the Sahlgrenska Academy, Division of Endocrinology, Department of Internal Medicine, Göteborg University, Gröna stråket 8 SE-413 45 Göteborg, Sweden
Department of Rheumatology and Inflammation Research at the Sahlgrenska Academy, Göteborg University, Guldhedsgatan 10, SE-413 46 Göteborg, Sweden
Department of Physiology, Göteborg University, Medicinaregatan 9, Box 434 SE-405 30 Göteborg, Sweden
Department of Pharmacology, Göteborg University, Medicinaregatan 9, Box 434 SE-405 30 Göteborg, Sweden

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It is generally believed that estrogens exert their bone sparing effects directly on the cells within the bone compartment. The aim of the present study was to investigate if central mechanisms might be involved in the bone sparing effect of estrogens. The dose–response of central (i.c.v) 17β-estradiol (E2) administration was compared with that of peripheral (s.c.) administration in ovariectomized (ovx) mice. The dose–response curves for central and peripheral E2 administration did not differ for any of the studied estrogen-responsive tissues, indicating that these effects were mainly peripheral. In addition, ovx mice were treated with E2 and/or the peripheral estrogen receptor antagonist ICI 182,780. ICI 182,780 attenuated most of the estrogenic response regarding uterus weight, retroperitoneal fat weight, cortical BMC and trabecular bone mineral content (P<0.05). These findings support the notion that the primary target tissue that mediates the effect of E2 on bone is peripheral and not central.

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