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

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.

1974 ◽  
Vol 52 (5) ◽  
pp. 972-977
Author(s):  
Claude L. Morin ◽  
Jean Léveillé ◽  
Victor Ling

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.


1965 ◽  
Vol 65 (1) ◽  
pp. 15-19 ◽  
Author(s):  
M. R. McRoberts ◽  
R. Hill ◽  
A. C. Dalgarno

1. The teeth of sheep that had been fed from 6 months of age for 12 months on diets low in calcium or in phosphorus and vitamin D content were compared with those of similar animals fed a control diet.2. The low calcium diet depressed the development of both dentine and enamel but had a greater effect on enamel than dentine, while the low phosphorus and vitamin D diet depressed dentine development slightly and had practically no effect on enamel.3. The percentages of ash of the dentine and enamel were not significantly affected by the diets fed.


Endocrinology ◽  
2007 ◽  
Vol 148 (3) ◽  
pp. 1396-1402 ◽  
Author(s):  
Yurong Song ◽  
James C. Fleet

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.


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

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

1975 ◽  
Vol 49 (5) ◽  
pp. 481-484
Author(s):  
M. Kaye

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.


1996 ◽  
Vol 270 (1) ◽  
pp. R11-R21 ◽  
Author(s):  
M. G. Tordoff

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.


Sign in / Sign up

Export Citation Format

Share Document