Effect of Oophorectomy and Calcium Deprivation on Bone Mass in the Rat

1978 ◽  
Vol 54 (4) ◽  
pp. 439-446 ◽  
Author(s):  
A. Hodgkinson ◽  
Jean E. Aaron ◽  
A. Horsman ◽  
M. S. F. McLachlan ◽  
B. E. C. Nordin
Keyword(s):  
Bone Mass ◽  
Trabecular Bone ◽  
Dry Weight ◽  
Calcium Deficiency ◽  
Normal Diet ◽  
Female Rats ◽  
Cross Sectional ◽  
Calcium Diet ◽  
Low Calcium Diet ◽  
Low Calcium

1. The effects of a low calcium diet and of oophorectomy, separately and together, on cortical and trabecular bone mass, have been examined in mature female rats. 2. Calcium deprivation caused a significant decrease of weight, cortical cross-sectional area and ratio of cortical to total area in the femur, it significantly reduced the volume of trabecular bone and increased the percentage of osteoid surface in the tail vertebrae, and in addition increased the urinary excretion of phosphate and, initially, of hydroxyproline. 3. Oophorectomy caused similar though smaller changes in trabecular bone and urine, whereas the effects of oophorectomy on cortical bone were greater on a low calcium intake than on a normal intake. 4. The ash weight of the femora, expressed as a percentage of the total dry weight, was unaffected by calcium deprivation or oophorectomy alone but was significantly reduced when the two occurred together. 5. The percentage of resorption surfaces in the vertebrae tended to increase on the low calcium diet and after oophorectomy on the normal diet but decreased after oophorectomy on a low calcium diet. 6. It is concluded that oophorectomy and calcium deficiency each reduce bone mass in the adult rat but the greatest effect is seen when they are combined.

scholarly journals Lack of Insulin-Like Growth Factor I Exaggerates the Effect of Calcium Deficiency on Bone Accretion in Mice

Endocrinology ◽  
2003 ◽  
Vol 144 (11) ◽  
pp. 4682-4689 ◽  
Author(s):  
Yuji Kasukawa ◽  
David J. Baylink ◽  
Jon E. Wergedal ◽  
Yousef Amaar ◽  
Apurva K. Srivastava ◽  
...  
Keyword(s):  
Calcium Deficiency ◽  
Growth Phases ◽  
Active Growth ◽  
Dihydroxyvitamin D ◽  
1,25 Dihydroxyvitamin D ◽  
Calcium Diet ◽  
Low Calcium Diet ◽  
Low Calcium ◽  
Igf I ◽  
Normal Calcium

Abstract Recent studies provide evidence that the GH/IGF-I axis plays a critical role in the regulation of bone accretion that occurs during puberty and that the peak bone mineral density (BMD) is dependent on the amount of dietary calcium intake during the active growth phases. To evaluate whether IGF-I deficiency exaggerates the effect of calcium deficiency on bone accretion during active growth phases, IGF-I knockout (KO) and wild-type (WT) mice were fed with low calcium (0.01%) or normal calcium (0.6%) for 2 wk during the pubertal growth phase and were labeled with tetracycline. The low calcium diet caused significant decreases in endosteal bone formation parameters and a much greater increase in the resorbing surface of both the endosteum and periosteum of the tibia of IGF-I KO mice compared with WT mice. Accordingly, femur BMD measured by dual energy x-ray absorptiometry or peripheral quantitative computed tomography increased significantly in IGF-I WT mice fed the low calcium diet, but not in IGF-I KO mice. IGF-I-deficient mice fed the normal calcium diet showed elevated PTH levels, decreased serum 1,25-dihydroxyvitamin D and serum calcium levels at baseline. Serum calcium changes due to calcium deficiency were greater in IGF-I KO mice compared with WT mice. PTH levels were 7-fold higher in IGF-I KO mice fed normal calcium compared with WT mice, which was further elevated in mice fed the low calcium diet. Treatment of IGF-I-deficient lit/lit mice with GH decreased the serum PTH level by 70% (P < 0.01). Based on these and past findings, we conclude that: 1) IGF-I deficiency exaggerates the negative effects of calcium deficiency on bone accretion; and 2) IGF-I deficiency may lead to 1,25-dihydroxyvitamin D deficiency and elevated PTH levels even under normal calcium diet.

scholarly journals Serum biomarkers of the calcium-deficient rats identified by metabolomics based on UPLC/Q-TOF MS/MS

2020 ◽  
Author(s):  
Meng Fanyu ◽  
Fan Lina ◽  
Sun Lin ◽  
Yu Qingli ◽  
Maoqing Wang ◽  
...  
Keyword(s):  
Calcium Deficiency ◽  
Diet Group ◽  
Nutritional Rickets ◽  
Calcium Diet ◽  
Low Calcium Diet ◽  
Low Calcium ◽  
Metabolomics Study ◽  
Diagnostic Values ◽  
Metabolic Profiling Analysis ◽  
Tof Ms

Abstract Background: We previously identified the urinary biomarkers to diagnose calcium deficiency and nutritional rickets by ultra-performance liquid chromatography/quadrupole time-of-flight tandem mass spectrometry (UPLC/Q-TOF MS/MS).To further confirm these biomarkers in vivo, we performed serum metabolomics analysis of calcium deficiency.Methods: A calcium-deficient rat model was established with a low-calcium diet for 12 weeks. Serum-metabolomics-based UPLC/Q-TOF MS/MS and multivariate statistical analysis was performed to identify the alterations in metabolites associated with calcium deficiency in rats.Results: Bone mineral density, serum parathyroid hormone and alkaline phosphatase were significantly decreased in the low-calcium diet group (LCG) compared to the normal calcium diet group (NCG). Serum metabolic-profiling analysis could definitively distinguish between the LCG and NCG andidentified25 calcium-deficient biomarkers. Three metabolites (indoxyl sulfate, phosphate, and taurine) of the 25 biomarkers were found in our previous urinary metabolomics study of rats with a calcium deficiency and nutritional rickets. The areas under the curve (AUCs) of these three biomarkers were greater than 0.8, and the combination of any two biomarkers was higher than 0.95.Conclusion: Dietary calcium deficiency induced the alterations of metabolites in the serum of rats, and the three identified biomarkers had relatively high diagnostic values for calcium deficiency in rats.hatase were significantly decreased in the low-calcium diet group (LCG) compared to the normal calcium diet group (NCG). Serum metabolic-profiling analysis could definitively distinguish between the LCG and NCG andidentified25 calcium-deficient biomarkers. Three metabolites (indoxyl sulfate, phosphate, and taurine) of the 25 biomarkers were found in our previous urinary metabolomics study of rats with a calcium deficiency and nutritional rickets. The areas under the curve (AUCs) of these three biomarkers were greater than 0.8, and the combination of any two biomarkers was higher than 0.95. Conclusion Dietary calcium deficiency induced the alterations of metabolites in the serum of rats, and the three identified biomarkers had relatively high diagnostic values for calcium deficiency in rats.

scholarly journals Serum biomarkers of the calcium-deficient rats identified by metabolomics based on UPLC/Q-TOF MS/MS

2020 ◽  
Author(s):  
Meng Fanyu ◽  
Fan Lina ◽  
Sun Lin ◽  
Yu Qingli ◽  
Maoqing Wang ◽  
...  
Keyword(s):  
Calcium Deficiency ◽  
Diet Group ◽  
Mineral Density ◽  
Nutritional Rickets ◽  
Calcium Diet ◽  
Low Calcium Diet ◽  
Low Calcium ◽  
Serum Metabolomics ◽  
Tof Ms

Abstract Background We previously identified the urinary biomarkers to diagnose calcium deficiency and nutritional rickets by ultra-performance liquid chromatography/quadrupole time-of-flight tandem mass spectrometry (UPLC/Q-TOF MS/MS).To further confirm these biomarkers in vivo, we performed serum metabolomics analysis of calcium deficiency. Methods A calcium-deficient rat model was established with a low-calcium diet for 12 weeks. Serum-metabolomics-based UPLC/Q-TOF MS/MS and multivariate statistical analysis was performed to identify the alterations in metabolites associated with calcium deficiency in rats. Results Bone mineral density, serum parathyroid hormone and alkaline phosphatase were significantly decreased in the low-calcium diet group (LCG) compared to the normal calcium diet group (NCG). Serum metabolic-profiling analysis could definitively distinguish between the LCG and NCG andidentified25 calcium-deficient biomarkers. Three metabolites (indoxyl sulfate, phosphate, and taurine) of the 25 biomarkers were found in our previous urinary metabolomics study of rats with a calcium deficiency and nutritional rickets. The areas under the curve (AUCs) of these three biomarkers were greater than 0.8, and the combination of any two biomarkers was higher than 0.95. Conclusion Dietary calcium deficiency induced the alterations of metabolites in the serum of rats, and the three identified biomarkers had relatively high diagnostic values for calcium deficiency in rats.

scholarly journals Serum biomarkers of the calcium-deficient rats identified by metabolomics based on UPLC/Q-TOF MS/MS

2019 ◽  
Author(s):  
Fanyu Meng ◽  
Lina Fan ◽  
Lin Sun ◽  
Qingli Yu ◽  
Maoqing Wang ◽  
...  
Keyword(s):  
Calcium Deficiency ◽  
Diet Group ◽  
Mineral Density ◽  
Nutritional Rickets ◽  
Calcium Diet ◽  
Low Calcium Diet ◽  
Low Calcium ◽  
Serum Metabolomics ◽  
Tof Ms

Abstract Background: We previously identified the urinary biomarkers to diagnose calcium deficiency and nutritional rickets by ultra-performance liquid chromatography/quadrupole time-of-flight tandem mass spectrometry (UPLC/Q-TOF MS/MS).To further confirm these biomarkers in vivo, we performed serum metabolomics analysis of calcium deficiency. Methods: A calcium-deficient rat model was established with a low-calcium diet for 12 weeks. Serum-metabolomics-based UPLC/Q-TOF MS/MS and multivariate statistical analysis was performed to identify the alterations in metabolites associated with calcium deficiency in rats. Results: Bone mineral density, serum parathyroid hormone and alkaline phosphatase were significantly decreased in the low-calcium diet group (LCG) compared to the normal calcium diet group (NCG). Serum metabolic-profiling analysis could definitively distinguish between the LCG and NCG and identified25 calcium-deficient biomarkers. Three metabolites (indoxyl sulfate, phosphate, and taurine) of the 25 biomarkers were found in our previous urinary metabolomics study of rats with a calcium deficiency and nutritional rickets. The areas under the curve (AUCs) of these three biomarkers were greater than 0.8, and the combination of any two biomarkers was higher than 0.95. Conclusion: Dietary calcium deficiency induced the alterations of metabolites in the serum of rats, and the three identified biomarkers had relatively high diagnostic values for calcium deficiency in rats.

scholarly journals THE EFFECT OF EXPERIMENTAL REDUCTION OF KIDNEY SUBSTANCE UPON THE PARATHYROID GLANDS AND SKELETAL TISSUE

1936 ◽  
Vol 64 (6) ◽  
pp. 965-980 ◽  
Author(s):  
Alwin M. Pappenheimer ◽  
Keyword(s):  
Dietary Calcium ◽  
Calcium Deficiency ◽  
Renal Tissue ◽  
Parathyroid Glands ◽  
Skeletal Tissue ◽  
Young Rats ◽  
Calcium Diet ◽  
Low Calcium Diet ◽  
Low Calcium ◽  
Dietary Calcium Deficiency

Reduction of renal tissue in young rats regularly leads to a marked increase in the volume of the parathyroid glands. If partially nephrectomized rats are maintained on a low calcium diet, growth is stunted, and skeletal lesions are produced, of far greater severity than can be ascribed to the dietary calcium deficiency alone. The picture closely resembles that found in cases of renal rickets in children.

scholarly journals Effect of low-calcium diet and grind diet on bone turnover of ovariectomized female rats

2011 ◽  
pp. e497-e502 ◽  
Author(s):  
GP. Costa ◽  
DS. Leite ◽  
RF. do Prado ◽  
VAS. Silveira ◽  
YR. Carvalho
Keyword(s):  
Bone Turnover ◽  
Female Rats ◽  
Calcium Diet ◽  
Low Calcium Diet ◽  
Low Calcium

scholarly journals Interplay among calcium diet content, PTH(1-34) treatment and balance of bone homeostases in rat model: the trabecular bone as keystone

2019 ◽  
Author(s):  
Marzia Ferretti ◽  
Francesco Cavani ◽  
Laura Roli ◽  
Marta Checchi ◽  
Maria Sara Magarò ◽  
...  
Keyword(s):  
Bone Mass ◽  
Trabecular Bone ◽  
Rat Model ◽  
Immunohistochemical Analysis ◽  
Normal Diet ◽  
Second Step ◽  
Calcium Diet ◽  
Skeletal Homeostasis ◽  
Vertebral Bodies

The present study is the second step (concerning the normal-diet restoration) of the our previous one (concerning the calcium-free diet) to determine whether the normal-diet restoration, with/without concomitant PTH(1-34) administration, can influence amounts and deposition sites of the total bone mass. Histomorphometric evaluations and immunohistochemical analysis for Sclerostin expression were conducted on the vertebral bodies and femurs  in rat model. The final goals are: i) to define timing and manners of bone mass changes when calcium is restored in the diet; ii) to analyze the different involvement of the two bony architectures having different metabolism (i.e. trabecular versus cortical bone); iii) to verify the eventual role of PTH(1-34) administration. Results evidenced the greater involvement of the trabecular bone with respect to the cortical one, in answering to different calcium diet content, and the effect of PTH mostly in the recovery of trabecular bony architecture. The main findings emerged from the present study are: i) the importance of the interplay between mineral homeostasis and skeletal homeostasis in modulating and guiding bone answers to dietary/metabolic alterations and ii) the evidence that the more involved bony architecture is the trabecular one, the most susceptible to the dynamical balance of the two homeostases.

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