Abstract

To determine whether the uterus plays any role in mediating the ability of estrogen to conserve bone in the rat, eight groups of animals (n = 8) with their skeletons labeled with 45Ca were studied. Rats were ovariectomized (OVX), hysterectomized (Hyst), or given sham operations (Sham) and then pair-fed a low-hydroxyproline casein diet for 4 weeks. The groups were treated orally with 17 beta-estradiol (E2) or vehicle, and serial measurements of biochemical markers of bone breakdown were made in weeks 1, 2, and 4. The femur density was measured by dual-energy X-ray absorptiometry (DXA), and skeletal calcium and 45Ca content were determined chemically. Final total body calcium values (mg) in the eight treatment groups were (means +/- SD): Sham, 2573 +/- 179; Sham + E2, 2635 +/- 159; Hyst, 2537 +/- 151; Hyst + E2, 2410 +/- 151; OVX, 2189 +/- 146; OVX + E2, 2559 +/- 172; OVX/Hyst, 2138 +/- 132; and OVX/Hyst + E2, 2460 +/- 140. Ovariectomy raised biochemical markers of bone resorption (urinary 45Ca, hydroxyproline, and deoxypyridinoline), lowered DXA bone mineral density, and reduced total body calcium and 45Ca content in both Hyst and Sham-Hyst animals (p < 0.001), whereas E2 treatment prevented these changes. Hysterectomy did not impair the ability of E2 to conserve bone in OVX rats. Thus, we conclude that estrogen-mediated induction of growth factors from uterine tissue does not play an essential role in mediating the bone-conserving actions of estrogen in the rat.

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