{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2024,8,16]],"date-time":"2024-08-16T05:11:17Z","timestamp":1723785077856},"reference-count":36,"publisher":"Oxford University Press (OUP)","issue":"7","license":[{"start":{"date-parts":[[1996,7,1]],"date-time":"1996-07-01T00:00:00Z","timestamp":836179200000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/journals\/pages\/open_access\/funder_policies\/chorus\/standard_publication_model"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[1996,7,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:p>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\u03b2-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 \u00b1 SD): Sham, 2573 \u00b1 179; Sham + E2, 2635 \u00b1 159; Hyst, 2537 \u00b1 151; Hyst + E2, 2410 \u00b1 151; OVX, 2189 \u00b1 146; OVX + E2, 2559 \u00b1 172; OVX\/Hyst, 2138 \u00b1 132; and OVX\/Hyst + E2, 2460 \u00b1 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 &amp;lt; 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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