Arnino Acid Transport by Rat Parathyroid Glands in vivo: Effect of Low Calcium Diet.

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.

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

10.21203/rs.2.19585/v1 ◽

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.

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

Journal of Experimental Medicine ◽

10.1084/jem.64.6.965 ◽

1936 ◽

Vol 64 (6) ◽

pp. 965-980 ◽

Cited By ~ 38

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.

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ROLE OF THE PARATHYROID GLANDS IN THE ENHANCEMENT OF INTESTINAL CALCIUM ABSORPTION IN RESPONSE TO A LOW CALCIUM DIET

Journal of Endocrinology ◽

10.1677/joe.0.0740345 ◽

1977 ◽

Vol 74 (3) ◽

pp. 345-354 ◽

Cited By ~ 12

Author(s):

J. FOX ◽

R. SWAMINATHAN ◽

T. M. MURRAY ◽

A. D. CARE

Keyword(s):

Small Intestine ◽

Calcium Binding ◽

Calcium Absorption ◽

Binding Protein ◽

Calcium Binding Protein ◽

Intestinal Calcium Absorption ◽

Parathyroid Glands ◽

Calcium Diet ◽

Low Calcium Diet ◽

Low Calcium

SUMMARY The phenomenon of adaptation of intestinal calcium absorption to changes in dietary calcium has been studied in conscious pigs with Thiry–Vella jejunal loops. The result of decreasing the calcium content of the diet from 1·2 to 0·1% was an increase in the efficiency of the net absorption of calcium from the fluid used to perfuse the jejunal loop; this increase took place 4–6 days after the change in diet. A similar effect was noted in four pigs which had previously been parathyroidectomized and in two thyroparathyroidectomized pigs with thyroxine replacement therapy. The effect seen in the parathyroidectomized animals was not attributable to an increase in the concentration gradient of calcium ions between the jejunal lumen and the blood after the change to the low calcium diet. There was a marked increase in the amount of calcium-binding protein in the mucosa taken from the distal three-quarters of the small intestine of intact pigs fed a low calcium diet. However, after parathyroidectomy, the level of calcium in the diet had no significant effect on the amount of calcium-binding protein in the small intestine. It is concluded that, in pigs, neither parathyroid hormone nor calcitonin is necessary for intestinal adaptation to a low calcium diet and that, although this adaptation may be mediated by 1,25-dihydroxycholecalciferol, a significant increase in the level of calcium-binding protein in the intestine is only seen when the parathyroid glands are intact.

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

10.21203/rs.3.rs-29598/v2 ◽

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.

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Icariin protects against cage layer osteoporosis by intervening in steroid biosynthesis and glycerophospholipid metabolism

Animal Diseases ◽

10.1186/s44149-021-00001-z ◽

2021 ◽

Vol 1 (1) ◽

Author(s):

Zhengwang Yu ◽

Jie Huang ◽

Zhongxin Zhou

Keyword(s):

Metabolic Diseases ◽

Chinese Herb ◽

Therapeutic Effects ◽

Mineral Density ◽

Steroid Biosynthesis ◽

Metabolic Pathway Analysis ◽

Effective Prevention ◽

Calcium Diet ◽

Low Calcium Diet ◽

Low Calcium

AbstractCage layer osteoporosis (CLO) is a common bone metabolism disease in the breeding industry of China. However, effective prevention for CLO has not been developed. Icariin (ICA), the main bioactive component of the Chinese herb Epimedium, has been shown to have good therapeutic effects on bone-related diseases. In this study, the effects of ICA were further evaluated in a low-calcium diet-induced CLO, and a serum metabolomics assay was performed to understand the underlying mechanisms. A total of 144 31-wk-old Lohmann pink-shell laying hens were randomly allocated to 4 groups with 6 replicates of 6 hens per replicate. The 4 dietary treatment groups consisted of a basal diet (3.5% calcium), a low-calcium diet (2.0% calcium), and a low-calcium diet supplemented with 0.5 or 2.0 g/kg ICA. The results showed that ICA exerted good osteoprotective effects on low-calcium diet-induced CLO. ICA significantly increased femur bone mineral density, improved bone microstructure, decreased bone metabolic level, and upregulated mRNA expression of bone formation genes in femoral bone tissue. Serum untargeted metabolomics analysis showed that 8 metabolite levels were significantly changed after ICA treatment, including increased contents of 7-dehydrocholesterol, 7-oxocholesterol, desmosterol, PC (18:1(9Z)/18:1(9Z)), PS (18:0/18:1(9Z)), N,N-dimethylaniline and 2-hydroxy-butanoic acid and decreased N2,N2-dimethylguanosine. Metabolic pathway analysis based on the above 8 metabolites indicated that ICA mainly perturbed steroid biosynthesis and glycerophospholipid metabolism. These findings suggest that ICA can effectively prevent bone loss in low-calcium diet-induced CLO by mediating steroid biosynthesis and glycerophospholipid metabolism and provide new information for the regulation of bone metabolic diseases.

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