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Excessive vitamin D content of a standard iron-deficient diet for rats

Published online by Cambridge University Press:  25 March 2008

Stella M. Triggs
Affiliation:
Departments of Pathology and Haematology, Welsh National School of Medicine, Health Park, Cardiff CF4 4XN
R. Bailey
Affiliation:
Departments of Pathology and Haematology, Welsh National School of Medicine, Health Park, Cardiff CF4 4XN
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Abstract

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1. The observation that thyroid C cell hyperplasia occurred in rats given the iron-deficient diet described by McCall, Newman, O'Brien, Valberg & Witts (1962) prompted a closer study of the preparation and constituents of this diet..

2. It became apparent that there was a discrepancy between the amounts of fat-soluble vitamins in the dietary formulation reported and the supposed final content of the diet. A diet prepared as described by McCall et al. (1962) contains 1000 μg (40000 i.u.) ergocalciferol and 10 μg (14 500 i.u.) retinyl palmitate/kg..

3. An experiment was designed to study the effect of Fe-deficient and Fe-supplemented, high-vitamin-D diets, and an Fe-supplemented, normal-vitamin-D diet, on thyroid C cell volume and serum calcium concentration..

4. Thyroid C cell volumes and serum Ca concentrations were significantly higher in both groups given excess vitamin D than in the group given the Fe-supplemented, normal-vitamin-D diet. It is evident therefore, that hypervitaminosis D was the cause of the morphological and biochemical changes found in rats given the McCall et al. (1962) diet.

Type
Papers on General Nutrition
Copyright
Copyright © The Nutrition Society 1976

References

Bailey-Wood, R., Blayney, L. M., Jacobs, A. & Muir, J. (1975). J. exp. Path. 56, 193.Google Scholar
Bannerman, R. M. (1965). J. Lab. clin. Med. 65, 944.Google Scholar
Bedard, Y. C., Pinkerton, P. H. & Simon, G. T. (1973). Blood 43, 131.CrossRefGoogle Scholar
Burns, D. G. & Spray, G. H. (1969). Br. J. Nutr. 23, 665.CrossRefGoogle Scholar
Croxton, F. E. (1959). Elementary Statistics, 2nd ed. New York: Dover.Google Scholar
Dallman, P. R. (1969). J. Nutr. 97, 475.CrossRefGoogle Scholar
Dencker, L. & Tjälve, H. (1973). Experientia 29, 719.CrossRefGoogle Scholar
Gindler, E. M. & King, J. D. (1972). Am. J. clin. Path. 58, 376.CrossRefGoogle Scholar
Guldager, A. (1936). Hypervitaminosis D. Københaun, Norway: Nytt Nordisk Ferlag.Google Scholar
Haug, R. (1955). Z. Anat. EntwGesch. 118, 302.CrossRefGoogle Scholar
McCall, M. G., Newman, G. E., O'Brien, J. R. P., Valberg, L. S. & Witts, L. J. (1962). Br.J. Nutr. 16, 297CrossRefGoogle Scholar
Richmond, V. S., Worwood, M. & Jacobs, A. (1972). Br. J. Haemat. 23, 605.CrossRefGoogle Scholar
Sørenson, E. W. (1965). Acta med. scand. 178, 385.CrossRefGoogle Scholar
Spry, C. J. & Piper, K. G. (1969). Br. J. Nutr. 23, 91.CrossRefGoogle Scholar
Stux, M., Thomson, B., Isler, H. & Leblond, C. D. (1961). Endocrinology, 68, 385.CrossRefGoogle Scholar
Thomson, A. B., Shaver, C., Lee, D. J., Jones, B. J. & Valdberg, L. S. (1971). Am. J. Physiol. 220, 674.CrossRefGoogle Scholar
Triggs, S. M. (1974). Studies on the role of dietary factors in the induction of tumours of the thyroid and parathyroid. PhD Thesis, University of Wales.Google Scholar