scholarly journals Vitamin D Metabolites in Plasma of Cows Fed a Prepartum Low-Calcium Diet for Prevention of Parturient Hypocalcemia

1981 ◽  
Vol 64 (2) ◽  
pp. 217-226 ◽  
Author(s):  
H.B. Green ◽  
R.L. Horst ◽  
D.C. Beitz ◽  
E.T. Littledike
Keyword(s):  
Vitamin D ◽  
Vitamin D Metabolites ◽  
Calcium Diet ◽  
Low Calcium Diet ◽  
Low Calcium

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.

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 III. The composition and structure of the teeth. III. The composition and structure of the teeth

1965 ◽  
Vol 65 (1) ◽  
pp. 15-19 ◽  
Author(s):  
M. R. McRoberts ◽  
R. Hill ◽  
A. C. Dalgarno
Keyword(s):  
Vitamin D ◽  
Control Diet ◽  
Calcium Diet ◽  
Low Calcium Diet ◽  
Low Calcium ◽  
Composition And Structure ◽  
Low Phosphorus

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.

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 The Role of Zinc, Copper and Calcium in the Etiology of the "Meat Anemia"

Blood ◽  
1964 ◽  
Vol 23 (6) ◽  
pp. 786-794 ◽  
Author(s):  
KARL GUGGENHEIM
Keyword(s):  
Vitamin D ◽  
Intestinal Tract ◽  
Genetic Factors ◽  
Toxic Effects ◽  
Calcium Diet ◽  
Low Calcium Diet ◽  
Low Calcium ◽  
Copper Supplementation ◽  
High Treatment

Abstract The suggestion that the "meat anemia" of mice is due to a dietary lack of copper accompanied by an excess of zinc in meat was investigated. Muscle meat contains small amounts of copper and much more zinc whereas liver which protects against "meat anemia" contains more copper and less zinc than muscle. Supplementation of meat with copper or liver, which reduce the zinc-copper ratio of the diet, prevents anemia. Addition of zinc, which increases the zinc-copper ratio, leads to anemia. Calcium prevents anemia even when the zinc-copper ratio is high. Treatment with vitamin D does not protect against anemia. It is concluded that calcium acts before its absorption in the intestinal tract, probably by interfering with the absorption of zinc. Anemia also develops in mice which are maintained on a semisynthetic low-calcium diet with a higher content of zinc than of copper. Supplementation of this diet with calcium likewise alleviates the anemia. Rats, which are resistant to "meat anemia," are less susceptible to the toxic effects of zinc than mice. "Meat anemia" of mice seems, therefore, to result mainly from the presence in meat of insufficient amounts of copper accompanied by an excess of zinc, the effects of which are accentuated by a concomitant lack of calcium. Genetic factors determining the particular sensitivity to zinc seem to play an important role as well.

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