SKELETAL METABOLISM IN ESTROGEN-TREATED RATS STUDIED BY MEANS OF Ca<sup>45</sup><sup>1</sup>

Lindquist, Bertil; Budy, Ann M.; McLean, Franklin C.; Howard, J.

doi:10.1210/endo-66-1-100

Cited by 48 publications

(19 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…These results were explained by assuming that during the 120 minute period after 45Ca injection, there would be relatively little 45Ca returning to the plasma from bone, so that the 45Ca content in bone would reflect the bone uptake of calcium. This agreed with the fact that estrogen (Lindquist et al, 1960, Riggs et al, 1969 and ethanol have been shown to have no effect on calcium uptake by bone (Krishnamra and Limlomwongse, 1983). When the plasma 45Ca level (cpm/0.1 ml) was examined 18 hr after 45Ca ip administration , it reflected an exchange of calcium between plasma and bone fluid (Doppelt and Talmage, 1976).…”

Section: Discussionsupporting

confidence: 68%

“…Estrogen has been known to suppress bone resorption in post-menopausal women (Riggs et al,_ 1969 and and in rat (Lindquist et al, 1960) possibly by reducing the sensitivity of bone to PTH (Heany 1965, Jasani et al, 1965, Nordin 1970, Atkins et al, 1972, Orimo et al, 1972. In the present studies, estrogen administration was also shown to reduce bone resorption in ovariectomized rats to the normal value as seen in group II (Figure 2).…”

Section: Discussionsupporting

confidence: 68%

“…The primary effect of estrogen appears to be the inhibition of bone resorption (Lindquist et al, 1960, Riggs et al, 1969 but the mean by which estrogen exerts its effect upon bone remains unclear. It has been suggested that estrogen decreases the responsiveness of bone to parathyroid hormone (PTH) (Heaney 1965, Jasani et al, 1965, Nordin et al, 1970, Atkins et al, 1972, Orimo et al, 1972and Riggs et al, 1972.…”

mentioning

confidence: 99%

See 2 more Smart Citations

Calcium metabolism in relation to chronic ethanol ingestion and estrogen deficiency in rat.

1983

View full text Add to dashboard Cite

AbstractsThe plasma calcium concentration, urinary calcium excretion, total bone calcium content and the rate of calcium uptake and release by tibias were measured in 6 groups of rats which were kept under various treatment protocols for 8 wk. Ovariectomy led to significant hypocalcemia and a decrease in bone calcium content the former being reversed towards normal by estrogen treatment.Chronic ethanol ingestion reduced the bone calcium content without apparent effect on plasma calcium in intact rat and further reduced (P<0.05) the bone calcium content in ovariectomized rats. The calcium uptake by the bone measured by 45Ca injected ip at zero hour was the same among the 6 groups. When "Ca was injected ip 17 hours earlier, the disappearance of plasma 45Ca was found to be slower in ovariectomized and alcohol treated groups, indicating a higher rate of calcium movement from bone to plasma. Moreover, there was also an increase in the rate of calcium release by tibias after ovariectomy and chronic alcohol ingestion ; the release was slightly greater in the condition of ovariectomy plus alcohol.The present investigation thus, provides evidence that ethanol is likely to have a direct stimulatory effect on bone resorption as well as an indirect effect through disrupting ovarian function during chronic administration.

show abstract

Section: Discussionsupporting

confidence: 68%

Section: Discussionsupporting

confidence: 68%

mentioning

confidence: 99%

See 1 more Smart Citation

Calcium metabolism in relation to chronic ethanol ingestion and estrogen deficiency in rat.

1983

View full text Add to dashboard Cite

show abstract

“…Estrogen prevents bone loss in this animal model by reducing bone turnover (18)(19)(20)(21)(22) while PTH, given intermittently, acts as an anabolic agent for bone formation (23)(24)(25)(26)(27)(28)(29). In this study, we present data on changes in bone mass, as well as trabecular connectivity, as a result oftreatment ofOvx animals with estrogen and/or PTH.…”

Section: Introductionmentioning

confidence: 97%

Loss of cancellous bone mass and connectivity in ovariectomized rats can be restored by combined treatment with parathyroid hormone and estradiol.

Shen¹,

Dempster²,

Birchman³

et al. 1993

J. Clin. Invest.

172

View full text Add to dashboard Cite

To evaluate the potential use of a combination of antiresorption and bone formation-promoting agents as a treatment for postmenopausal osteoporosis, we examined the effects of combined and separate administration of estrogen ( 17,8-estradiol, 30 ;Lg/ kg per d, s.c.) and parathyroid hormone (rPTH 40 ;&g/ kg per d, s.c.) on the proximal tibia of ovariectomized (Ovx) rats. The treatments lasted for 4 wk and were initiated 1, 3, and 5 wk after surgery. Ovx resulted in rapid loss of cancellous bone volume (Cn-BV/TV) as well as trabecular connectivity, as determined by two dimensional strut analysis. When administered in a preventive mode, treatment beginning I wk postOvx, estrogen or PTH treatment alone preserved Cn-BV/TV and trabecular connectivity, and combined estrogen and PTH treatment caused a 40% increment in Cn-BV/TV while maintaining comparable trabecular connectivity with that seen in the Sham-operated animals. When administered in a curative mode to rats with established osteoporosis, treatments beginning 3 or 5 wk post-Ovx, estrogen or PTH treatment alone prevented further loss of connectivity and Cn-BV/TV, whereas the combined treatment resulted in as much as a 300% improvement in one of the parameters of trabecular connectivity, node to node strut length, and a 106% increase in Cn-BV/TV, with respect to the bone status at the initiation of treatment. The beneficial effects of this combined treatment derive from estrogen's ability to prevent accelerated bone resorption and, simultaneously, PTH's promotion of bone formation. These data demonstrate, in an animal model, that therapies can be devised to cure the skeletal defects associated with established osteoporosis. (J.

show abstract

“…Experiments have demonstrated increased endosteal formation in mice (3), decreased endosteal resorption in rats (4), and no specific skeletal response in Received for publication 27 November 1968. kittens or in puppies (5). Also, if a defect in matrix synthesis is to be postulated, it is difficult to explain why neither castration nor protein restriction produces osteoporosis in experimental animals, although it can readily be produced by calcium deficiency (6,7), immobilization (8), or corticosteroid administration (9).…”

mentioning

confidence: 99%

Effect of sex hormones on bone in primary osteoporosis

Riggs¹,

Jowsey²,

Kelly³

et al. 1969

J. Clin. Invest.

200

View full text Add to dashboard Cite

A B S T R A C T The effect of sex hormones on bone tissue was studied in 12 osteoporotic patients. Surfaces of bone undergoing formation and resorption were determined by quantitative microradiography of iliac crest biopsy samples before and after treatment with estrogens in 11 postmenopausal women and with testosterone in one gonadally competent man. Before treatment, bone resorption was greater than normal in all but one patient and bone formation was normal. After treatment, bone resorption decreased to within the normal range in all patients, and bone formation did not change significantly. Biochemical studies showed significant decreases in serum calcium, phosphorus, and alkaline phosphatase levels and in urinary excretion of calcium and hydroxyproline. These changes are believed to be the consequence of the effect of the hormones on bone. The data indicate that the major effect of sex hormones in osteoporosis is an inhibition of bone resorption. INTRODUCTIONAlbright, Smith, and Richardson in 1941 proposed that anabolic sex hormones were necessary for bone matrix synthesis, and that the loss of estrogens at the menopause in women or of androgens with aging in men caused osteoporosis (1). Since then, sex hormones have been used extensively in the treatment of osteoporosis, although their mechanism of action and therapeutic usefulness have not been completely established.Estrogens stimulate intramedullary bone formation in birds (2), but their effect on mammalian bone is variable. Experiments have demonstrated increased endosteal formation in mice (3), decreased endosteal resorption in rats (4), and no specific skeletal response in

show abstract

SKELETAL METABOLISM IN ESTROGEN-TREATED RATS STUDIED BY MEANS OF Ca⁴⁵¹

Cited by 48 publications

References 0 publications

Calcium metabolism in relation to chronic ethanol ingestion and estrogen deficiency in rat.

Calcium metabolism in relation to chronic ethanol ingestion and estrogen deficiency in rat.

Loss of cancellous bone mass and connectivity in ovariectomized rats can be restored by combined treatment with parathyroid hormone and estradiol.

Effect of sex hormones on bone in primary osteoporosis

Contact Info

Product

Resources

About

SKELETAL METABOLISM IN ESTROGEN-TREATED RATS STUDIED BY MEANS OF Ca451

Cited by 48 publications

References 0 publications

Calcium metabolism in relation to chronic ethanol ingestion and estrogen deficiency in rat.

Calcium metabolism in relation to chronic ethanol ingestion and estrogen deficiency in rat.

Loss of cancellous bone mass and connectivity in ovariectomized rats can be restored by combined treatment with parathyroid hormone and estradiol.

Effect of sex hormones on bone in primary osteoporosis

Contact Info

Product

Resources

About

SKELETAL METABOLISM IN ESTROGEN-TREATED RATS STUDIED BY MEANS OF Ca⁴⁵¹