The Direct Effect of Calcium on the Hyperparathyroidism of Chronic Renal Failure

1975 ◽  
Vol 49 (5) ◽  
pp. 481-484
Author(s):  
M. Kaye
Keyword(s):  
Renal Failure ◽  
Chronic Renal Failure ◽  
Direct Effect ◽  
Bone Disease ◽  
Calcium Intake ◽  
Calcium Content ◽  
Calcium Diet ◽  
Low Calcium Diet ◽  
Low Calcium

1. The direct effect of calcium on the hyperparathyroidism of chronic renal failure was studied in rats with induced chronic renal failure, who were fed on a diet low in phosphate and who received supplemental phosphate by injection. They were given a normal (0·8%), or low (0·1%) or high (1·7%) calcium diet. 2. The animals on the low calcium diet had larger parathyroids and more severe bone disease at the end of 4 weeks, indicating the importance of calcium intake in directly influencing the degree of hyperparathyroidism. 3. Increasing the calcium content of the diet from 0·8% to 1·7% produced no additional benefits.

Administration of caseinomacropeptide-enriched extract to mice enhances the calcium content of femur in a low-calcium diet

2015 ◽  
Vol 44 ◽  
pp. 15-20 ◽  
Author(s):  
P. Burns ◽  
A. Binetti ◽  
P. Torti ◽  
U. Kulozik ◽  
L. Forzani ◽  
...  
Keyword(s):  
Calcium Content ◽  
Calcium Diet ◽  
Low Calcium Diet ◽  
Low Calcium

Adrenalectomy decreases NaCl intake of rats fed low-calcium diets

1996 ◽  
Vol 270 (1) ◽  
pp. R11-R21 ◽  
Author(s):  
M. G. Tordoff
Keyword(s):  
Salt Intake ◽  
Calcium Content ◽  
Calcium Diet ◽  
Low Calcium Diet ◽  
Low Calcium ◽  
High Salt Intake ◽  
High Calcium ◽  
Bone Content ◽  
Adrenocortical Hormone ◽  
Intact Rats

Five studies were conducted to characterize the effects on NaCl intake of the interaction between adrenalectomy (ADX) and dietary calcium. Intact rats fed low-calcium diets (0 or 25 mmol Ca2+/kg diet) approximately quadrupled intake of 300 or 500 mM NaCl solution relative to intact rats fed diets with moderate or high calcium content (125, 150, or 500 mmol Ca2+/kg diet) ADX approximately doubled NaCl intake of rats fed moderate or high-calcium diets but decreased NaCl intake of rats fed low-calcium diets to levels similar to those of ADX rats fed moderate of high-calcium diets. Aldosterone replacement (2.4 micrograms/day sc) reduced NaCl intake of ADX rats fed control diets to below levels of intact controls, but the same treatment to ADX rats fed low-calcium diet had no effect on NaCl intake. The reduction in NaCl intake produced by ADX in rats fed low-calcium diet could not be attributed to general debilitation, damage to the adrenal medulla, or altered metabolism of sodium or calcium (i.e., plasma concentration, bone content, or balance). It is proposed that an adrenocortical hormone other than aldosterone mediates the high salt intake of the calcium-deprived rat, and thus the adrenal has both inhibitory and excitatory actions on NaCl intake.

Effect of Vitamin D Deficiency on Aminoaciduria and Intestinal Transport of Amino Acids in the Rat

1974 ◽  
Vol 52 (5) ◽  
pp. 972-977
Author(s):  
Claude L. Morin ◽  
Jean Léveillé ◽  
Victor Ling
Keyword(s):  
Amino Acids ◽  
Vitamin D ◽  
Secondary Hyperparathyroidism ◽  
Vitamin D Deficiency ◽  
Intestinal Transport ◽  
Calcium Content ◽  
Calcium Diet ◽  
Low Calcium Diet ◽  
Low Calcium ◽  
Normal Calcium

Generalized hyperaminoaciduria and hyperphosphaturia are associated with human vitamin D deficiency rickets and the effect has been reproduced in animals. The basis for the renal transport impairment was attributed to secondary hyperparathyroidism resulting from hypocalcemia.In this study we attempted over a 16-week period to induce hyperaminoaciduria in Holtzman rats with vitamin D deficient diets of varying calcium content (0.4% and 0.04%) so as to investigate the possibility of a concomitant defect in intestinal transport of amino acids. Despite signs of secondary hyperparathyroidism, generalized hyperaminoaciduria was not in evidence in any of the groups. However, increased urinary excretion of lysine and taurine was demonstrated in rats fed a low calcium diet without vitamin D (LCa−D). The same observation was also made for taurine in rats deprived of vitamin D and on a normal calcium diet (NCa−D) and in animals fed a low calcium diet with vitamin D (LCa+D). The results failed to show any effect of vitamin D deficiency, hypocalcemia, or secondary hyperparathyroidism on the intestinal transport of lysine, alanine, and cycloleucine.

Regulation of intestinal calcium-binding protein calcium intake in the rat

1975 ◽  
Vol 228 (3) ◽  
pp. 861-869 ◽  
Author(s):  
T Freund ◽  
F Bronner
Keyword(s):  
Calcium Intake ◽  
Calcium Binding ◽  
Calcium Concentration ◽  
Binding Protein ◽  
Calcium Binding Protein ◽  
Competitive Binding Assay ◽  
Calcium Diet ◽  
Low Calcium Diet ◽  
Low Calcium ◽  
High Calcium

Analytical gel electrophoresis of the vitamin D-dependent intestinal calcium-binding protein (CaBP) has demonstrated two protein bands (1 and 2) of similar molecular weight and similar specific binding activity. The mucosal concentration of CaBP, measured by a quantitative competitive binding assay, has been shown to vary reproducibly and inversely with calcium intake and the mucosal calcium concentration. These same factors also influence the relationship of bands 1 and 2. When animals on a high-calcium diet were placed on a low-calcium diet, their CaBP increased by 35% in 24 h and by 48% in 48 h and reached a level typical of animals on a low-calcium diet. Measurement of the diurnal variation of CaBP and mucosal calcium in animals allowed access to feed only at night revealed significant, but inverse, oscillations. These observations are interpreted as reflecting a regulation of CaBP by the mucosal calcium concentration, which appears to reflect absorbed calcium in transit.

Calcium transport in the ileum of uremic rats

1982 ◽  
Vol 242 (2) ◽  
pp. G128-G134
Author(s):  
M. Koller ◽  
U. Binswanger
Keyword(s):  
Renal Failure ◽  
Calcium Transport ◽  
Dihydroxyvitamin D3 ◽  
Calcium Diet ◽  
Low Calcium Diet ◽  
Low Calcium ◽  
Unidirectional Fluxes ◽  
Small Intestinal ◽  
Normal Calcium

Duodenal and ileal calcium transport was studied by 45Ca uptake and estimation of unidirectional fluxes in vitro in kidney-intact and 5/6-nephrectomized rats. After normal-calcium diet, calcium transport was impaired by uremia in the duodenum but not in the ileum. However, 5/6-nephrectomized rats on low-calcium diet showed, in concert with impaired growth, a reduced calcium transport both in duodenum and ileum. Comparing data after normal- and low-calcium diets, the ileal adaptation to low-calcium diet was intact in mild renal failure but abolished in severe uremia (urea less than 100 mg/dl). These results suggest that ileal calcium transport after normal-calcium diet is mainly passive. Taking into account reduced food intake as an additional factor, the active ileal calcium transport after low-calcium diet declines with progressive renal failure according to decreasing levels of 1,25-dihydroxyvitamin D3. A suspected enhancement of the distal small intestinal calcium transport by parathyroid hormone in uremic rats as compensation for proximally impaired absorption could not be demonstrated.

The effects of diets deficient in phosphorus, phosphorus and vitamin D, or calcium, on the skeleton and teeth of the growing sheep. II. Malocclusion of the teeth

1965 ◽  
Vol 65 (1) ◽  
pp. 11-14 ◽  
Author(s):  
M. R. McRoberts ◽  
R. Hill ◽  
A. C. Dalgarno
Keyword(s):  
Vitamin D ◽  
Mineral Content ◽  
Treatment Effects ◽  
Control Diet ◽  
Calcium Content ◽  
Calcium Diet ◽  
Low Calcium Diet ◽  
Low Calcium ◽  
Molar Teeth

1. In growing sheep fed on a low-calcium diet for 12 months and for a similar period on a diet of adequate mineral content, a tendency for the incisor teeth to protrude beyond the maxillary pad (prognathism) was observed. This arose primarily during the repair period, and was apparently caused by poorer repair of the upper skull than of the mandible. This was not observed in animals fed on a control diet or one deficient in phosphorus and vitamin D.2. A malocclusion of molar teeth associated with poorly mineralized and extremely weak mandibles, which prevented the incisor teeth from meeting the dental pad, occurred in growing sheep fed for 12 months on a diet deficient in phosphorus and vitamin D. This defect was not observed in similar animals fed on a control diet nor in those fed on a diet of low calcium content. Treatment effects on the shape of the mandible that were apparently related to this malocclusion are described.

scholarly journals AMMONIUM CHLORIDE DECALCIFICATION, AS MODIFIED BY CALCIUM INTAKE: THE RELATION BETWEEN GENERALIZED OSTEOPOROSIS AND OSTITIS FIBROSA

1932 ◽  
Vol 56 (6) ◽  
pp. 823-834 ◽  
Author(s):  
Henry L. Jaffe ◽  
Aaron Bodansky ◽  
Joseph P. Chandler
Keyword(s):  
Ammonium Chloride ◽  
Calcium Intake ◽  
Age Groups ◽  
Von Recklinghausen’S Disease ◽  
Calcium Diet ◽  
Low Calcium Diet ◽  
Low Calcium ◽  
Underlying Causes ◽  
Ostitis Fibrosa ◽  
Marrow Fibrosis

1. In all age groups the effects of ammonium chloride administration were found to be strikingly dependent upon the calcium intake. 2. Dogs receiving an adequate calcium diet and ammonium chloride showed less decalcification than those receiving a low calcium diet with or without ammonium chloride. 3. In the younger groups the added effect of ammonium chloride to calcium-low diet brought out more striking changes than a low calcium diet alone. 4. When the decalcification was less severe—in the oldest dogs on the low calcium diet with or without ammonium chloride, and in the younger dogs on an adequate calcium intake with ammonium chloride —generalized thinning of the bones without marrow fibrosis resulted (osteoporosis). 5. When the decalcification was rapid and severe—in the youngest dogs on low calcium diet, particularly with ammonium chloride— generalized decalcification and secondary marrow fibrosis resulted (ostitis fibrosa). 6. Generalized ostitis fibrosa is a rather inclusive term and may be applied to the histologic picture which results when clinical or experimental decalcification is rapid, and therefore leads to extensive marrow fibrosis. 7. The special underlying causes of the decalcification may incidentally contribute features to modify the generalized osteoporosis or ostitis fibrosa as in rickets and in von Recklinghausen's disease.

A comparison of some methods of supplying calcium to intensively kept chicks

1946 ◽  
Vol 36 (3) ◽  
pp. 199-206 ◽  
Author(s):  
D. J. G. Black
Keyword(s):  
Live Weight ◽  
Calcium Content ◽  
Weight Basis ◽  
Food Utilization ◽  
Calcium Diet ◽  
Low Calcium Diet ◽  
Low Calcium ◽  
Normal Calcium

1. An experiment was performed to compare some methods of supplying calcium to intensively kept chickens.2. The calcium content of a mash was adjusted to contain low (0·13%), normal (1·16%) and high (2·14%) amounts, and each of these mashes was fed to groups of chicks having access to: (a) no grit, (b) flint grit alone, (c) limestone grit alone, (d) both flint and limestone grit.3. The addition of flint grit significantly improved the efficiency of food utilization on all diets, whether limestone grit was provided or not.4. On all three mashes the total amount of calcium grit consumed was greater in the presence of flint grit than when it was fed alone.5. As the level of calcium in the diet increased, the amount of limestone grit consumed decreased, whether it was fed alone or in the presence of flint grit.6. The best results, judged on a live-weight basis, were obtained when the normal calcium mash was fed with flint grit alone, followed by the low calcium mash with both flint and limestone grit, followed by the normal calcium mash with no grit.7. On the basis of the efficiency of food utilization, the low calcium diet with flint and limestone grit was best followed by the normal calcium diet with flint grit alone.8. Access to limestone grit reduced the efficiency of food utilization in all but the low calcium diet.

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

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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