scholarly journals Persistence of 1,25D-induced hypercalciuria in alendronate-treated genetic hypercalciuric stone-forming rats fed a low-calcium diet

2014 ◽  
Vol 306 (9) ◽  
pp. F1081-F1087 ◽  
Author(s):  
Kevin K. Frick ◽  
John R. Asplin ◽  
Christopher D. Culbertson ◽  
Ignacio Granja ◽  
Nancy S. Krieger ◽  
...  
Keyword(s):  
Vitamin D ◽  
Bone Density ◽  
Bone Resorption ◽  
Mrna Expression ◽  
Kidney Stones ◽  
Sprague Dawley ◽  
Vitamin D Receptors ◽  
Low Calcium Diet ◽  
Renal Tubular ◽  
Intestinal Ca Absorption

Genetic hypercalciuric stone-forming (GHS) rats demonstrate increased intestinal Ca absorption, increased bone resorption, and reduced renal tubular Ca reabsorption leading to hypercalciuria and all form kidney stones. GHS have increased vitamin D receptors (VDR) at these sites of Ca transport. Injection of 1,25(OH)2D3 (1,25D) leads to a greater increase in urine (u)Ca in GHS than in control Sprague-Dawley (SD), possibly due to the additional VDR. In GHS the increased uCa persists on a low-Ca diet (LCD) suggesting enhanced bone resorption. We tested the hypothesis that LCD, coupled to inhibition of bone resorption by alendronate (alen), would eliminate the enhanced 1,25D-induced hypercalciuria in GHS. SD and GHS were fed LCD and half were injected daily with 1,25D. After 8 days all were also given alen until euthanasia at day 16. At 8 days, 1,25D increased uCa in SD and to a greater extent in GHS. At 16 days, alen eliminated the 1,25D-induced increase in uCa in SD. However, in GHS alen decreased, but did not eliminate, the 1,25D-induced hypercalciuria, suggesting maximal alen cannot completely prevent the 1,25D-induced bone resorption in GHS, perhaps due to increased VDR. There was no consistent effect on mRNA expression of renal transcellular or paracellular Ca transporters. Urine CaP and CaOx supersaturation (SS) increased with 1,25D alone in both SD and GHS. Alen eliminated the increase in CaP SS in SD but not in GHS. If these results are confirmed in humans with IH, the use of bisphosphonates, such as alen, may not prevent the decreased bone density observed in these patients.

scholarly journals 1,25(OH)2D3-enhanced hypercalciuria in genetic hypercalciuric stone-forming rats fed a low-calcium diet

2013 ◽  
Vol 305 (8) ◽  
pp. F1132-F1138 ◽  
Author(s):  
Kevin K. Frick ◽  
John R. Asplin ◽  
Nancy S. Krieger ◽  
Christopher D. Culbertson ◽  
Daniel M. Asplin ◽  
...  
Keyword(s):  
Bone Resorption ◽  
Bone Cells ◽  
Idiopathic Hypercalciuria ◽  
Sprague Dawley ◽  
Vitamin D Receptors ◽  
Low Calcium Diet ◽  
Calcium Reabsorption ◽  
Renal Tubular ◽  
Intestinal Ca Absorption ◽  
Tubular Calcium Reabsorption

The inbred genetic hypercalciuric stone-forming (GHS) rats exhibit many features of human idiopathic hypercalciuria and have elevated levels of vitamin D receptors (VDR) in calcium (Ca)-transporting organs. On a normal-Ca diet, 1,25(OH)2D3 (1,25D) increases urine (U) Ca to a greater extent in GHS than in controls [Sprague-Dawley (SD)]. The additional UCa may result from an increase in intestinal Ca absorption and/or bone resorption. To determine the source, we asked whether 1,25D would increase UCa in GHS fed a low-Ca (0.02%) diet (LCD). With 1,25D, UCa in SD increased from 1.2 ± 0.1 to 9.3 ± 0.9 mg/day and increased more in GHS from 4.7 ± 0.3 to 21.5 ± 0.9 mg/day ( P < 0.001). In GHS rats on LCD with or without 1,25D, UCa far exceeded daily Ca intake (2.6 mg/day). While the greater excess in UCa in GHS rats must be derived from bone mineral, there may also be a 1,25D-mediated decrease in renal tubular Ca reabsorption. RNA expression of the components of renal Ca transport indicated that 1,25D administration results in a suppression of klotho, an activator of the renal Ca reabsorption channel TRPV5, in both SD and GHS rats. This fall in klotho would decrease tubular reabsorption of the 1,25D-induced bone Ca release. Thus, the greater increase in UCa with 1,25D in GHS fed LCD strongly suggests that the additional UCa results from an increase in bone resorption, likely due to the increased number of VDR in the GHS rat bone cells, with a possible component of decreased renal tubular calcium reabsorption.

scholarly journals The combination of miacalcic, calcium lactate, and vitamin C as postextracted alveolar bone resorption inhibitor

2010 ◽  
Vol 43 (3) ◽  
pp. 141
Author(s):  
Sri Kentjananingsih
Keyword(s):  
Vitamin D ◽  
Bone Density ◽  
Bone Resorption ◽  
Vitamin C ◽  
Group Treatment ◽  
Alveolar Bone ◽  
Vitamin D Supplementation ◽  
Calcium Lactate ◽  
Control Group ◽  
Significant Difference

Background: Tooth extraction can cause alveolar resorption, and will reduce the denture retention. The process of bone resorption looks like the process of osteoporosis. Calcium and vitamin D supplementation is the rational therapy for minimizing bone loss. Miacalcic is the drug of choice for osteporotic patient. Purpose: This study is aimed to know whether the combination of miacalcic, calcium lactate, and vitamin C are effective in inhibiting post extracted alveolar resorption. Methods: Thirty three healthy postmenopausal women were chosen as samples and they were classified randomly into control group (without treatment), 1st experiment group (treatment was started 3 months post extraction), and 2nd experiment group (treatment was started at the 2nd day post extraction). The treatment was done by giving miacalcic nasal spray, calcium lactate 500 mg and vitamin C 100 mg tablets every morning in 10 days every month for 3 months. X-ray photo of the post extracted area were taken an hour, 3 months, and 6 months post-extraction. Results: After 6 month, there was significant difference in buccolingual thickness decreasing among three groups (p<0.05). The maximum mean difference of buccolingual thickness decreasing was 0.72 mm, between control and 2nd experiment groups. There was no significant difference about decreasing bone density among them (p>0.10). The maximum difference of the mean of density decreasing was 1,906 g/cm2/mm between control and 2nd experiment groups. The increasing density mostly occurred in the 2nd experiment group. Conclusion: The combination of miacalcic, calcium lactate, and vitamin C are effective for inhibiting alveolar resorption, although statistically there was no significant difference about bone density decreasing. The sooner this treatment is given the better result will be achieved.Latar belakang: Pencabutan gigi menyebabkan resorpsi tulang alveolaris, dan akan mengurangi retensi geligi tiruan. Proses resorpsi tulang alveol pada osteoporosis mirip dengan proses resorpsi tulang pada penyembuhan luka bekas pencabutan. Miacalcic adalah obat utama untuk penderita osteoporosis. Kalsium dan vitamin D merupakan terapi yang rasional untuk meminimalkan resorpsi tulang. tujuan: Membuktikan apakah kombinasi miacalcic, kalsium laktat, and vitamin C juga efektif menghambat resorpsi tulang alveol pasca pencabutan. Metode: Sampel 33 wanita postmenopause yang sehat, terbagi secara acak ke dalam kelompok kontrol (tanpa perlakuan), kelompok eksperimen 1 (perlakuan mulai 3 bulan pasca pencabutan) dan kelompok eksperimen 2 (perlakuan mulai hari kedua pasca pencabutan). Perlakuannya yaitu: pemberian miacalcic semprot hidung, tablet kalsium laktat 500 mg dan vitamin C 100 mg setiap pagi, 10 hari dalam sebulan, selama tiga bulan. Foto sinar-X dari regio pasca pencabutan dibuat satu jam, 3 bulan, dan 6 bulan pasca pencabutan. Hasil: 6 bulan pasca-cabut, ada beda bermakna perihal selisih tebal bukolingual tulang alveol antar ketiga kelompok (p<0,05). Rerata penurunan ketebalan ini maksimal sebanyak 0.72 mm, antara kelompok kontrol dan kelompok eksperimen 2. Penurunan kepadatan tulang antar ketiga kelompok tidak bermakna (p>0,10). Beda maksimum rerata kepadatan tulang antara kelompok kontrol dan kelompok eksperimen 2 sebesar 1,906 g/cm2/mm. Peningkatan kepadatan terbanyak dialami anggota kelompok eksperimen 2. Kesimpulan: Kombinasi miacalcic, kalsium laktat, vitamin C efektif menghambat resorpsi tulang alveolaris, walaupun secara statistik beda penurunan kepadatan tidak bermakna. Makin awal pemberian perlakuan, hasilnya akan lebih baik.

Increased sensitivity to 1,25(OH)2D3 in bone from genetic hypercalciuric rats

1996 ◽  
Vol 271 (1) ◽  
pp. C130-C135 ◽  
Author(s):  
N. S. Krieger ◽  
V. M. Stathopoulos ◽  
D. A. Bushinsky
Keyword(s):  
Bone Resorption ◽  
Calcium Absorption ◽  
Immunoblot Analysis ◽  
Calcium Excretion ◽  
Sprague Dawley ◽  
Urine Calcium ◽  
Fourfold Increase ◽  
Low Calcium Diet ◽  
Slot Blot Analysis ◽  
Urine Calcium Excretion

As a model of human hypercalciuria, we have selectively inbred genetic hypercalciuric stone-forming (GHS) Sprague-Dawley rats whose mean urine calcium excretion is eight to nine times greater than that of controls. A large component of this excess urine calcium excretion is secondary to increased intestinal calcium absorption, which is not due to an elevation in serum 1,25(OH)2D3, but appears to result from an increased number of intestinal 1,25(OH)2D3 receptors (VDR). When GHS rats are fed a low-calcium diet, the hypercalciuria is only partially decreased and urine calcium excretion exceeds intake, suggesting that an additional mechanism contributing to the hypercalciuria is enhanced bone demineralization. To determine if GHS rat bones are more sensitive to exogenous 1,25(OH)2D3, we cultured calvariae from neonatal (2- to 3-day-old) GHS and control rats with or without 1,25(OH)2D3 or parathyroid hormone (PTH) for 48 h at 37 degrees C. There was significant stimulation of calcium efflux from GHS calvariae at 1 and 10 nM 1,25(OH)2D3, whereas control calvariae showed no significant response to 1,25(OH)2D3 at any concentration tested. In contrast, PTH induced similar bone resorption in control and GHS calvariae. Immunoblot analysis demonstrated a fourfold increase in the level of VDR in GHS calvariae compared with control calvariae, similar to the increased intestinal receptors described previously. There was no comparable change in VDR RNA levels as measured by slot blot analysis, suggesting the altered regulation of the VDR occurs posttranscriptionally. That both bone and intestine display an increased amount of VDR suggests that this may be a systemic disorder in the GHS rat and that enhanced bone resorption may be responsible, in part, for the hypercalciuria in the GHS rat.

scholarly journals Comparison of the Pharmacological Effects of Paricalcitol and Doxercalciferol on the Factors Involved in Mineral Homeostasis

2010 ◽  
Vol 2010 ◽  
pp. 1-8 ◽  
Author(s):  
J. Ruth Wu-Wong ◽  
Masaki Nakane ◽  
Gerard D. Gagne ◽  
Kristin A. Brooks ◽  
William T. Noonan
Keyword(s):  
Vitamin D ◽  
Cell Proliferation ◽  
Mrna Expression ◽  
Active Form ◽  
Parathyroid Cell ◽  
Pharmacological Effects ◽  
Sprague Dawley ◽  
Mineral Homeostasis ◽  
Sprague Dawley Rats ◽  
Serum Pth

Vitamin D receptor agonists (VDRAs) directly suppress parathyroid hormone (PTH) mRNA expression. Different VDRAs are known to have differential effects on serum calcium (Ca), which may also affect serum PTH levels since serum Ca regulates PTH secretion mediated by the Ca-sensing receptor (CaSR). In this study, we compared the effects of paricalcitol and doxercalciferol on regulating serum Ca and PTH, and also the expression of PTH, VDR, and CaSR mRNA. The 5/6 nephrectomized (NX) Sprague-Dawley rats on a normal or hyperphosphatemia-inducing diet were treated with vehicle, paricalcitol, or doxercalciferol for two weeks. Both drugs at the tested doses (0.042–0.33 g/kg) suppressed PTH mRNA expression and serum PTH effectively in the 5/6 NX rats, but paricalcitol was less potent in raising serum Ca than doxercalciferol. In pig parathyroid cells, paricalcitol and the active form of doxercalciferol induced VDR translocation from the cytoplasm into the nucleus, suppressed PTH mRNA expression and inhibited cell proliferation in a similar manner, although paricalcitol induced the expression of CaSR mRNA more effectively. The multiple effects of VDRAs on modulating serum Ca, parathyroid cell proliferation, and the expression of CaSR and PTH mRNA reflect the complex involvement of the vitamin D axis in regulating the mineral homeostasis system.

scholarly journals Differential expression of protein disulfide-isomerase A3 isoforms, PDIA3 and PDIA3N, in human prostate cancer cell lines representing different stages of prostate cancer

2021 ◽  
Author(s):  
Maria Araceli Diaz Cruz ◽  
Sandra Karlsson ◽  
Ferenc Szekeres ◽  
Maria Faresjö ◽  
Dan Lund ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Vitamin D ◽  
Mrna Expression ◽  
Cell Lines ◽  
Protein Function ◽  
Protein Disulfide Isomerase ◽  
Expression Ratio ◽  
Disulfide Isomerase ◽  
Vitamin D Receptors ◽  
Protein Disulfide

AbstractProstate cancer (PCa) is a highly heterogeneous and unpredictable progressive disease. Sensitivity of PCa cells to androgens play a central role in tumor aggressiveness but biomarkers with high sensitivity and specificity that follow the progression of the disease has not yet been verified. The vitamin D endocrine system and its receptors, the Vitamin D Receptor (VDR) and the Protein Disulfide-Isomerase A3 (PDIA3), are related to anti-tumoral effects as well as carcinogenesis and have therefore been suggested as potential candidates for the prevention and therapy of several cancer forms, including PCa. In this study, we evaluated the mRNA expression of VDR and PDIA3 involved in vitamin D signaling in cell lines representing different stages of PCa (PNT2, P4E6, LNCaP, DU145 and PC3). This study further aimed to evaluate vitamin D receptors and their isoforms as potential markers for clinical diagnosis of PCa. A novel transcript isoform of PDIA3 (PDIA3N) was identified and found to be expressed in all PCa cell lines analyzed. Androgen-independent cell lines showed a higher mRNA expression ratio between PDIA3N/PDIA3 contrary to androgen-dependent cell lines that showed a lower mRNA expression ratio between PDIA3N/PDIA3. The structure of PDIA3N differed from PDIA3. PDIA3N was found to be a N-truncated isoform of PDIA3 and differences in protein structure suggests an altered protein function i.e. cell location, thioredoxin activity and affinity for 1,25(OH)2D3. Collectively, PDIA3 transcript isoforms, the ratio between PDIA3N/PDIA3 and especially PDIA3N, are proposed as candidate markers for future studies with different stages of PCa progression.

scholarly journals Role for ovarian hormones in purinoceptor-dependent natriuresis

2020 ◽  
Author(s):  
Eman Gohar ◽  
Malgorzata Kasztan ◽  
Shali Zhang ◽  
Edward W Inscho ◽  
David M Pollock
Keyword(s):  
Mrna Expression ◽  
Collecting Duct ◽  
Premenopausal Women ◽  
Renal Medulla ◽  
Receptor Protein ◽  
Protein Abundance ◽  
Sprague Dawley ◽  
Ovx Rats ◽  
Downstream Effectors ◽  
Renal Tubular

Abstract Background: Premenopausal women have a lower risk of hypertension compared to age-matched men and postmenopausal women. P2Y2 and P2Y4 purinoceptor can be considered potential contributors to hypertension due to their emerging roles in regulating renal tubular Na+ transport. Activation of these receptors inhibits epithelial Na+ channel activity (ENaC) via a phospholipase C (PLC)-dependent pathway resulting in natriuresis. We recently reported that activation of P2Y2 and P2Y4 receptors in the renal medulla by UTP promotes natriuresis in male and ovariectomized (OVX) rats, but not in ovary-intact females. This led us to hypothesize that ovary-intact females have greater basal renal medullary activity of P2 (P2Y2 and P2Y4) receptors regulating Na+ excretion compared to male and OVX rats. Methods: To test our hypothesis, we determined (i) the effect of inhibiting medullary P2 receptors by suramin (750 μg/kg/min) on urinary Na+ excretion in anesthetized male, ovary-intact female and OVX Sprague Dawley rats, (ii) mRNA expression and protein abundance of P2Y2 and P2Y4 receptors and (iii) mRNA expression of their downstream effectors (PLC-1d and ENaCa) in renal inner medullary tissues obtained from these three groups. We also subjected cultured mouse inner medullary collecting duct cells (segment 3, mIMCD3) to different concentrations of 17ß-estradiol (E2, 0, 10, 100 and 1000 nM) to test whether E2 increases mRNA expression of P2Y2 and P2Y4 receptors.Results: Acute P2 inhibition attenuated urinary Na+ excretion in ovary-intact females, but not in male or OVX rats. We found that P2Y2 and P2Y4 mRNA expression was higher in the inner medulla from females compared to males or OVX. Inner medullary lysates showed that ovary-intact females have higher P2Y2 receptor protein abundance, compared to males, however, OVX did not eliminate this sex difference. We also found that E2 dose-dependently upregulated P2Y2 and P2Y4 mRNA expression in mIMCD3. Conclusion: These data suggest that ovary-intact females have enhanced P2Y2 and P2Y4-dependent regulation of Na+ handling in the renal medulla, compared to male and OVX rats. We speculate that the P2 pathway contributes to facilitated renal Na+ handling in premenopausal females.

scholarly journals Role for ovarian hormones in purinoceptor-dependent natriuresis

2020 ◽  
Author(s):  
Eman Gohar ◽  
Malgorzata Kasztan ◽  
Shali Zhang ◽  
Edward W Inscho ◽  
David M Pollock
Keyword(s):  
Mrna Expression ◽  
Collecting Duct ◽  
Premenopausal Women ◽  
Renal Medulla ◽  
Receptor Protein ◽  
Na Channel ◽  
Protein Abundance ◽  
Sprague Dawley ◽  
Ovx Rats ◽  
Renal Tubular

Abstract Background: Premenopausal women have a lower risk of hypertension compared to age-matched men and postmenopausal women. P2Y 2 and P2Y 4 purinoceptor can be considered potential contributors to hypertension due to their emerging roles in regulating renal tubular Na + transport. Activation of these receptors inhibits epithelial Na + channel activity (ENaC) via a phospholipase C (PLC)-dependent pathway resulting in natriuresis. We recently reported that activation of P2Y 2 and P2Y 4 receptors in the renal medulla by UTP promotes natriuresis in male and ovariectomized (OVX) rats, but not in ovary-intact females. This led us to hypothesize that ovary-intact females have greater basal renal medullary activity of P2 (P2Y 2 and P2Y 4 ) receptors regulating Na + excretion compared to male and OVX rats. Methods: To test our hypothesis, we determined (i) the effect of inhibiting medullary P2 receptors by suramin (750 μg/kg/min) on urinary Na + excretion in anesthetized male, ovary-intact female and OVX Sprague Dawley rats, (ii) mRNA expression and protein abundance of P2Y 2 and P2Y 4 receptors and (iii) mRNA expression of their downstream effectors (PLC-1d and ENaCa) in renal inner medullary tissues obtained from these three groups. We also subjectedcultured mouse inner medullary collecting duct cells (segment 3, mIMCD3) to different concentrations of 17ß-estradiol(E 2 , 0, 10, 100 and 1000 nM) to test whether E 2 increases mRNA expression of P2Y 2 and P2Y 4 receptors. Results: Acute P2 inhibition attenuated urinary Na + excretion in ovary-intact females, but not in male or OVX rats.We found that P2Y 2 and P2Y 4 mRNA expression was higher in the inner medulla from females compared to males or OVX. Inner medullary lysates showed that ovary-intact females have higher P2Y 2 receptor protein abundance, compared to males, however, OVX did not eliminate this sex difference. We also found that E 2 dose-dependently upregulated P2Y 2 and P2Y 4 mRNA expression in mIMCD3. Conclusion: These data suggest that females have enhanced P2Y 2 and P2Y 4 -dependent regulation of Na + handling in the renal medulla, compared to male and OVX rats. We speculate that the P2 pathway contributes to facilitated renal Na + handling in premenopausal females.

scholarly journals Increased biological response to 1,25(OH)2D3 in genetic hypercalciuric stone-forming rats

2013 ◽  
Vol 304 (6) ◽  
pp. F718-F726 ◽  
Author(s):  
Kevin K. Frick ◽  
John R. Asplin ◽  
Murray J. Favus ◽  
Christopher Culbertson ◽  
Nancy S. Krieger ◽  
...  
Keyword(s):  
Transient Receptor Potential ◽  
Biological Response ◽  
Receptor Potential ◽  
K Channel ◽  
Transient Receptor Potential Vanilloid ◽  
Sprague Dawley ◽  
Vitamin D Receptors ◽  
Transient Receptor ◽  
Calbindin D ◽  
Intestinal Ca Absorption

Genetic hypercalciuric stone-forming (GHS) rats, bred to maximize urine (U) calcium (Ca) excretion, have increased intestinal Ca absorption and bone Ca resorption and reduced renal Ca reabsorption, leading to increased UCa compared with the Sprague-Dawley (SD) rats. GHS rats have increased vitamin D receptors (VDR) at each of these sites, with normal levels of 1,25(OH)2D3 (1,25D), indicating that their VDR is undersaturated with 1,25D. We tested the hypothesis that 1,25D would induce a greater increase in UCa in GHS rats by feeding both strains ample Ca and injecting 1,25D (25 ng · 100 g body wt−1 · day−1) or vehicle for 16 days. With 1,25D, UCa in SD increased from 1.7 ± 0.3 mg/day to 24.4 ± 1.2 (Δ = 22.4 ± 1.5) and increased more in GHS from 10.5 ± 0.7 to 41.9 ± 0.7 (Δ = 29.8 ± 1.8; P = 0.003). To determine the mechanism of the greater increase in UCa in GHS rats, we measured kidney RNA expression of components of renal Ca transport. Expression of transient receptor potential vanilloid (TRPV)5 and calbindin D28K were increased similarly in SD + 1,25D and GHS + 1,25D. The Na+/Ca2+ exchanger (NCX1) was increased in GHS + 1,25D. Klotho was decreased in SD + 1,25D and GHS + 1,25D. TRPV6 was increased in SD + 1,25D and increased further in GHS + 1,25D. Claudin 14, 16, and 19, Na/K/2Cl transporter (NKCC2), and secretory K channel (ROMK) did not differ between SD + 1,25D and GHS + 1,25D. Increased UCa with 1,25D in GHS exceeded that of SD, indicating that the increased VDR in GHS induces a greater biological response. This increase in UCa, which must come from the intestine and/or bone, must exceed any effect of 1,25D on TRPV6 or NCX1-mediated renal Ca reabsorption.

The growing interest in vitamin D is positively related to that of its kidney complications and is negatively related to that of bone benefit: an analysis based on Google Trends (Preprint)

2020 ◽  
Author(s):  
Marco Zaffanello
Keyword(s):  
Vitamin D ◽  
Bone Density ◽  
Vitamin D3 ◽  
Kidney Stones ◽  
Kidney Failure ◽  
Cardiovascular Health ◽  
Economic Status ◽  
Google Trends ◽  
Vitamin D2 ◽  
Electronic Search

BACKGROUND The benefits of vitamin D relate to muscle strength, cardiovascular health, and prevents osteoporosis. OBJECTIVE This study aimed to explore trends of global interest on vitamin D, hypercalcaemia, adverse kidney effects (stones and kidney failure) and osteoporosis METHODS An electronic search was conducted with Google Trends, limiting searches based on the "health" criterion. RESULTS Worldwide interest in vitamin D3 (cholecalciferol), vitamin D2 (ergocalciferol or calciferol), kidney stones and kidney failure is progressively growing over time. On the other hand, vitamin D was found to be negatively correlated with hypercalcaemia and bone density. Another result of our analysis is the distribution of the popularity of searches across countries. In particular, the global popularity for vitamin D3 seems higher than that of vitamin D2 and also shows different geographical preferences. The growing interest in vitamin D parallels that of kidney stones and kidney failure, while decreasing popularity has been noted for hypercalcaemia and bone density CONCLUSIONS The research volumes help to clarify the changes in the trends of use of supplements and the development of their complications, according to the different geographical areas, socio-economic status and online literacy

Effect of adrenal steroids on bone resorption in rats

1976 ◽  
Vol 230 (1) ◽  
pp. 90-93 ◽  
Author(s):  
S Yasumura
Keyword(s):  
Bone Density ◽  
Bone Resorption ◽  
Serum Calcium ◽  
Adrenal Steroids ◽  
Calcium Diet ◽  
Inhibit Bone Resorption ◽  
Low Calcium Diet ◽  
Low Calcium ◽  
Radiographic Technique ◽  
Parathyroid Extract

Rats labeled with strontium-85 (85Sr) were rejected with adrenocortical steroids for 2 wk. The urinary-to-tibial (U/T) 85Sr ratio was used as an index of bone resorption. The glucocorticoids caused an inhibition of skeletal resorption, as judged by the 50% reduction in the U/T ratio, and decreased excretion of hydroxyproline. Thyroidal calcitonin levels were slightly elevated in glucocorticoid-treated animals, suggestive of a possible retardation of calcitonin release. The U/T ratios of thyroparathyroidectomized (TPTX) rats injected with corticosteroids were 50% of control values. The results indicate that glucocorticoids inhibit bone resorption independent of the action of calcitonin. Cortisol treatment increased the tibial density as measured by a radiographic technique. However, bone density was decreased and the U/T ratio increased in steroid-treated rats fed a low-calcium diet. In TPTX cortisol-treated rats, parathyroid extract (PTE) increased the U/T ratio and serum calcium but not to the degree observed in TPTX PTE-injected control animals. These experiments indicate that in rats glucocorticoids inhibit the rate of bone resorption but this effect can be overcome in part by PTE.

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