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.

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.

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 Intestinal Resistance to 1,25 Dihydroxyvitamin D in Mice Heterozygous for the Vitamin D Receptor Knockout Allele

Endocrinology ◽  
2007 ◽  
Vol 148 (3) ◽  
pp. 1396-1402 ◽  
Author(s):  
Yurong Song ◽  
James C. Fleet
Keyword(s):  
Vitamin D ◽  
Vitamin D Receptor ◽  
Time Course ◽  
Transient Receptor Potential ◽  
Gene Knockout ◽  
Mrna Levels ◽  
Wild Type ◽  
Calcium Diet ◽  
Low Calcium Diet ◽  
Low Calcium

We tested the hypothesis that low vitamin D receptor (VDR) level causes intestinal vitamin D resistance and intestinal calcium (Ca) malabsorption. To do so, we examined vitamin D regulated duodenal Ca absorption and gene expression [transient receptor potential channel, vallinoid subfamily member 6 (TRPV6), 24-hydroxylase, calbindin D9k (CaBP) mRNA, and CaBP protein] in wild-type mice and mice with reduced tissue VDR levels [i.e. heterozygotes for the VDR gene knockout (HT)]. Induction of 24-hydroxylase mRNA levels by 1,25 dihydroxyvitamin D3 [1,25(OH)2 D3] injection was significantly reduced in the duodenum and kidney of HT mice in both time-course and dose-response experiments. TRPV6 and CaBP mRNA levels in duodenum were significantly induced after 1,25(OH)2 D3 injection, but there was no difference in response between wild-type and HT mice. Feeding a low-calcium diet for 1 wk increased plasma PTH, renal 1α-hydroxylase (CYP27B1) mRNA level, and plasma 1,25(OH)2 D3, and this response was greater in HT mice (by 88, 55, and 37% higher, respectively). In contrast, duodenal TRPV6 and CaBP mRNA were not higher in HT mice fed the low-calcium diet. However, the response of duodenal Ca absorption and CaBP protein to increasing 1,25(OH)2 D3 levels was blunted by 40% in HT mice. Our data show that low VDR levels lead to resistance of intestinal Ca absorption to 1,25(OH)2 D3, and this resistance may be due to a role for the VDR (and VDR level) in the translation of CaBP.

The Effect of High Sodium Intake on Bone Mineral Content in Rats fed Normal Calcium or low Calcium Diet

1993 ◽  
Vol 84 (s28) ◽  
pp. 8P-9P ◽  
Author(s):  
A Y S Chan ◽  
P Poon ◽  
E L P Chan ◽  
S L M Fung ◽  
R Swaminathan
Keyword(s):  
Bone Mineral Content ◽  
Bone Mineral ◽  
Mineral Content ◽  
Sodium Intake ◽  
High Sodium ◽  
High Sodium Intake ◽  
Calcium Diet ◽  
Low Calcium Diet ◽  
Low Calcium ◽  
Normal Calcium

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

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.

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.

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.

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