Long-Term Prevention of Postmenopausal Osteoporosis by Œstrogen

Lindsay, Robert; Aitken, J. M.; Anderson, Levy; Hart, D.M.; Macdonald, E.; Clarke, A.

doi:10.1016/s0140-6736(76)92217-0

Cited by 921 publications

(191 citation statements)

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“…The reduction in the femur weight may be associated with the well known decrease in bone formation in the absence of estrogens. 26,27 The reduction in the weight of several organs with OVX indicates that normal estrogen levels are necessary for the normal growth of these organs. Rats used in the present experiment were relatively young animals (6 weeks) whose maturation was not complete.…”

Section: Body Composition In Ovariectomized Trained Ratsmentioning

confidence: 99%

Effects of physical training on body composition and organ weights in ovariectomized and hyperestrogenic rats

Shinoda

2002

Int J Obes

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OBJECTIVE:To investigate whether regular endurance-type exercise can benefit rats submitted to a model of ovariectomy (OVX)-induced obesity with or without estrogen replacement. SUBJECTS: OVX Sprague-Dawley rats were compared to an ovariectomized-estradiol-treated group (OVXE2) and a Shamoperated (Sham) group. Each of these groups were subdivided into a sedentary and a treadmill-trained (8 wk) group. DESIGN AND MEASUREMENTS: An experimental study in which various parameters, including fat depots, blood lipids and several organ weights were measured. RESULTS: Plasma levels of 17b-estradiol and uterus weights were significantly (P < 0.05) lower in OVX compared to Sham and significantly (P < 0.01) higher in OVXE2 (hyperestrogenic) compared to Sham rats. Body weights were significantly (P < 0.01) different among groups, in the following decreasing order: OVX, Sham and OVXE2. The average daily food intake and food efficiency were significantly (P < 0.01) increased in OVX compared to Sham, whereas estradiol treatment diminished this effect (P < 0.01). Exercise training did not alter any of the above-mentioned variables in any of the three estrogen groups. Mesenteric and subcutaneous fat weights were significantly (P < 0.01) increased by OVX. This increase was abolished by estrogen replacement or by exercise training. Exercise training also decreased fat weights in OVXE2 and Sham rats. OVX resulted in a decrease in the weights of several other tissues (femur, heart, lungs, liver and adrenal glands) while hyperestrogenic replacement resulted in an increase in weight of all measured tissues. Aside from fat depots, exercise training did not affect any of the tissue weights with the exception for an increase in the weight of the plantaris muscle and adrenal glands and a decrease in lung weight in all three estrogen groups. CONCLUSION: In OVX animals, exercise training may bring about positive changes in body composition (ie reduction in fat weights) despite an ovariectomy-induced increase in body weight.

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Section: Body Composition In Ovariectomized Trained Ratsmentioning

confidence: 99%

Effects of physical training on body composition and organ weights in ovariectomized and hyperestrogenic rats

Shinoda

2002

Int J Obes

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“…Postmenopausal osteoporosis is delayed or prevented by substitution with estrogens (1)(2)(3). The mechanism by which estrogens exert their effects on bone is unknown, although it is thought that, at least in part, they may inhibit bone resorption (3).…”

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Enhanced osteoblast proliferation and collagen gene expression by estradiol.

Ernst

Schmid

Froesch

1988

Proc. Natl. Acad. Sci. U.S.A.

194

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Estrogens play a crucial role in the development of postmenopausal osteoporosis. However, the mechanism by which estrogens exert their effects on bone is unknown. Postmenopausal osteoporosis is delayed or prevented by substitution with estrogens (1-3). The mechanism by which estrogens exert their effects on bone is unknown, although it is thought that, at least in part, they may inhibit bone resorption (3). Estrogens may affect bone cells directly or indirectly via systemic or local factors. In the adult, continuous bone formation and resorption (remodeling) are highly regulated to permit bone to exert its major functions, mechanical support and mineral homeostasis (4). Estrogens may either affect the concerted process of bone remodeling, or transmit or modify signals selectively inducing bone formation or bone resorption. These signals control proliferation, differentiation, and other functions of highly specialized cell types, osteoclasts and osteoblasts. The latter are responsible for bone formation and at the same time crucially regulate bone-resorbing osteoclasts (5). Despite the well-documented effects of estrogens on bone in vivo (1-3, 6), finding estrogen receptors in bone has been difficult (7, 8).To examine whether 17f-estradiol directly affects boneforming cells, we used rat osteoblast-like cells in vitro under strictly serum-free conditions as a model (9). In this culture system calvaria cells express characteristics of osteoblastlike cells, such as alkaline phosphatase activity and responsiveness to parathyroid hormone (in terms of cAMP), to a higher degree than identically prepared cells grown under conventional culture conditions. We found in long-term cultures that 17p8-estradiol (i) stimulates cell proliferation in a dose-dependent fashion and (ii) increases steady-state levels of mRNA encoding the al chain of type I procollagen. Thus, estrogens stimulate bone formation by a direct action on osteoblasts.MATERIALS AND METHODS Cell Culture. Calvaria of newborn rats (ZUR:SIV, formerly Sprague-Dawley) were sequentially digested with bacterial collagenase, and the released osteoblast-like cells were inoculated in serum-free viscous medium as described elsewhere (9). In brief, single cells were seeded at about 1.3 x 105 cells per culture dish (Falcon, 35 mm in diameter) in 1 ml of serum-free, viscous minimal essential medium alpha/ F-12 medium (1:1 mixture, both from GIBCO, without phenol red) containing 0.25% delipidated bovine serum albumin (Serva) and 0.8% methylcellulose (MeC) (Serva). Osteoblast-like cells remain selectively as cuboidal cells in MeC medium, sediment to the bottom of the dish, and are anchored by extracellular matrix domains, mainly type I collagen (9).17,3-Estradiol (Sigma), the biologically inactive stereoisomer 17a-estradiol (Sigma), and the antiestrogen transtamoxifen (Sigma) were added at the beginning of the culture period, which lasted for 19-21 days (370C, humidified atmosphere of 90% N2/5% C02/5% 02).Growth Curves. In MeC medium, osteoblast-like cells proliferate ...

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“…"-' 5 It also appears that time of initiation, and length and continuity of estrogen drug therapy influence rate and amount of bone loss. [16][17][18][19] Until recently, however, the effect of estrogen drug treatment in preventing the clinical outcomes of osteoporosis, such as hip fractures, had not been investigated. A recent study of medical records showed no significant protective effect of conjugated estrogen exposure of six months or longer upon the hip and distal radius fracture experience of 157 matched case-control pairs of postmenopausal females.…”

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confidence: 99%