Skeletal effects of parathyroid hormone (1–34) in ovariectomized rats with or without concurrent administration of salmon calcitonin

SUMMARY Plasma magnesium levels measured in rats from 16·5 to 21·5 days of gestation and during the first week after birth proved to be invariably higher in the foetus than in the mother. The highest level observed was in the 16·5-day-old foetus. A small decrease occurred between 16·5 and 17·5 days of gestation; thereafter the plasma magnesium level did not change until 19·5 days and then decreased between 19·5 and 21·5 days. After birth an increase in plasma magnesium occurred with suckling but then remained constant during the first week of life. Parathyroid hormone (0·25 USP unit/g) injected into 21·5-day-old foetuses had no effect on plasma magnesium levels from 0·5 to 24 h after injection. This dose was found to be very potent in raising plasma calcium values 4 h after injection. In the 3-day-old newborn rat this dose was similarly ineffective. Removal of the foetal parathyroid glands by decapitation at 17·5 days of gestation was followed by a decrease in plasma magnesium at 21·5 days of gestation. Parathyroid hormone (0·25 USP unit/g) injected into decapitated foetuses did not change the level of magnesium in the plasma. Salmon calcitonin (S-CT) at two doses (0·4 and 4 ng/g) produced no effect on plasma magnesium concentrations in 3-day-old newborn rats 3 h after injection; whereas at both doses, marked diminutions in plasma calcium and phosphate concentrations were observed. After injection of 40 ng S-CT/g, plasma magnesium decreased in 3-day-old newborn rats 3 h after injection. This dose was found to decrease plasma magnesium in the 19·5-day-old foetus and in the 20·5-day-old foetus. Before 19·5 days of gestation no effect was observed.

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Single-dose local administration of parathyroid hormone (1–34, PTH) with β-tricalcium phosphate/collagen (β-TCP/COL) enhances bone defect healing in ovariectomized rats

Journal of Bone and Mineral Metabolism ◽

10.1007/s00774-018-0906-3 ◽

2018 ◽

Vol 37 (1) ◽

pp. 28-35 ◽

Cited By ~ 5

Author(s):

Zhou-Shan Tao ◽

Wan-Shu Zhou ◽

Xin-Jing Wu ◽

Lin Wang ◽

Min Yang ◽

...

Keyword(s):

Single Dose ◽

Parathyroid Hormone ◽

Bone Defect ◽

Tricalcium Phosphate ◽

Ovariectomized Rats ◽

Local Administration ◽

Defect Healing ◽

Bone Defect Healing

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Estrogens and progestogens conserve bone in rats deficient in calcitonin and parathyroid hormone

AJP Endocrinology and Metabolism ◽

10.1152/ajpendo.1989.257.6.e903 ◽

1989 ◽

Vol 257 (6) ◽

pp. E903-E908

Author(s):

A. Goulding ◽

E. Gold

Keyword(s):

Parathyroid Hormone ◽

Bone Resorption ◽

Ovariectomized Rats ◽

Lower Plasma ◽

Urinary Hydroxyproline ◽

Dihydroxyvitamin D ◽

1,25 Dihydroxyvitamin D ◽

Thyroxine Replacement ◽

Total Body ◽

D Values

To examine the abilities of estrogens and progestogens to slow bone resorption and conserve bone in ovariectomized rats deficient in calcitonin (CT) or parathyroid hormone (PTH), nine groups of animals with 45Ca-labeled bones were studied for 12 wk. Rats were thyroidectomized (TX), parathyroidectomized (PTX), or given sham neck operations (Sham) and treated orally with either estrogen, 300 micrograms 17 beta-estradiol.kg body wt-1.wk-1; progestogen, 500 micrograms norethisterone acetate.kg body wt-1.wk-1; or placebo (Plac). The TX rats had parathyroid autografts and thyroxine replacement. In all surgical groups, estradiol (E2) and norethindrone (Nor) slowed urinary 45Ca excretion and conserved bone (P less than 0.001). However E2 lowered urinary hydroxyproline more than Nor. Total body Ca values (mg +/- SD) were Sham + Plac, 3,079 +/- 201; Sham + E2, 3,886 +/- 335; Sham + Nor, 3,567 +/- 459; TX + Plac, 3,123 +/- 159; TX + E2, 3,869 +/- 235; TX + Nor, 3,540 +/- 422; PTX + Sham, 3,067 +/- 249; PTX + E2, 3,775 +/- 414; PTX + Nor, 3,635 +/- 467. Importantly, E2 and Nor conserved bone as effectively in TX and PTX groups as in Sham rats, although the PTX rats had slower bone resorption and lower plasma 1,25-dihydroxyvitamin D values (P less than 0.001) than groups with intact parathyroids. We conclude that the effects of estrogens and progestogens to slow bone resorption and conserve bone are independent of CT and PTH. These findings appear relevant to the pathogenesis and treatment of postmenopausal osteoporosis.

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Estrogens and antiestrogens: actions and interactions with fluphenazine on food intake and body weight in rats

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.1993.264.6.r1214 ◽

1993 ◽

Vol 264 (6) ◽

pp. R1214-R1218 ◽

Cited By ~ 4

Author(s):

J. M. Gray ◽

S. Schrock ◽

M. Bishop

Keyword(s):

Body Weight ◽

Adipose Tissue ◽

Weight Gain ◽

Food Intake ◽

Ethinyl Estradiol ◽

Body Weight Gain ◽

Fatty Acid Synthetase ◽

Ovariectomized Rats ◽

Synthetase Activity ◽

Concurrent Administration

Treatment of ovariectomized rats for 3 days with 2 micrograms estradiol benzoate (E2B), 6 micrograms ethinyl estradiol, or 1-2 mg of either of the antiestrogens nafoxidine or tamoxifen led to similar decreases in food intake, body weight gain, adipose tissue lipoprotein lipase activity, and hepatic fatty acid synthetase activity, despite their different effects on uterine growth and induction of progestin receptors in pituitary and adipose tissue. Longer-term (2 wk) treatment with tamoxifen resulted in similar transient changes in food intake and body weight gain, as did treatment with E2B. Daily administration of 50 micrograms fluphenazine (FLU) led to significant decreases in body weight, although there was no change in food intake. Concurrent administration of FLU with either E2B or tamoxifen led to additive effects on body weight and food intake change. None of the treatments had any effect on in vitro binding of [3H]tamoxifen to antiestrogen binding sites in pooled hypothalamic-preoptic area samples.

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