Hostname: page-component-78c5997874-m6dg7 Total loading time: 0 Render date: 2024-11-09T07:23:57.612Z Has data issue: false hasContentIssue false
  • English
  • Français

The experimental production of vitamin B12 deficiency in the baboon (Papio cynocephalus). A 2-year study

Published online by Cambridge University Press:  24 July 2007

R. C Siddons
R. C Siddons
Affiliation:
Wellcome Trust Research Laboratories, PO Box 43640, Nairobi, Kenya
Rights & Permissions [Opens in a new window]

Abstract

Core share and HTML view are not available for this content. However, as you have access to this content, a full PDF is available via the ‘Save PDF’ action button.

1. The development of vitamin B12 deficiency, as indicated by the serum and liver vitamin B12 levels and the excretion of methylmalonic acid, was studied over a 2-year period in baboons (Papio cynocephalus) given a diet deficient in vitamin B12. The effects of partial hepatectomy and the inclusion of either ampicillin or sodium propionate in the diet on the rate of development of the deficiency were also studied.

2. The baboons had previously been fed on a mainly vegetarian diet. Their serum vitamin B12 levels were less than 100 ng/l and the mean liver vitamin B12 concentration was 0·56 μ/g. Similar serum and liver vitamin B12 levels were found in baboons given a purified diet supplemented with 1 μg vitamin B12/d, and marked increases in the serum and liver vitamin B12 levels occurred when the daily intake was increased to 2 μg.

3. The serum vitamin B12 levels decreased to less than 20 ng/l in all baboons given a vitamin B12-deficient diet.

4. The liver vitamin B12 concentration also decreased in all baboons given a deficient diet. At 9 months the lowest levels (0·20 μ/g) were found in partially hepatectomized baboons but subsequently baboons given the diet containing ampicillin had the lowest levels (0·11 μ/g).

5. The excretion of methylmalonic acid after a valine load was found to be inversely related to the liver vitamin B12 concentration. In the early part of the study, partially hepatectomized baboons excreted the highest amount but subsequently baboons given a diet containing ampicillin excreted the highest amount.

6. Increased formiminoglutamic acid excretion after a histidine load was observed in two baboons given a vitamin B12-deficient diet and in both baboons the liver folic acid concentration was low.

7. No haematological or neurological symptoms of the vitamin B12 deficiency were observed.

Type
Clinical and Human Nutrition
Information
British Journal of Nutrition , Volume 32 , Issue 2 , September 1974 , pp. 219 - 228
Copyright
Copyright © The Nutrition Society 1974

References

REFERENCES

Adams, J. F. (1968). Scand. J. Gastroenterol. 3, 145.Google Scholar
Banerjee, D. K. & Chatterjea, J. B. (1960). Br. med. J. ii, 992.CrossRefGoogle Scholar
Buchanan, J. M., Elford, H. L., Loughlin, R. E., McDougall, B. M. & Rosenthal, S. (1964). Ann. N. Y. Acad. Sci. 112, 756.CrossRefGoogle Scholar
Cardinale, G. J., Carty, T. J. & Abeles, R. H. (1970). J. biol. Chem. 245, 3771.CrossRefGoogle Scholar
Chanarin, I. & Bennett, M. C. (1962). Br. med. J. i, 27.CrossRefGoogle Scholar
Chanarin, I., Hutchinson, M., McClean, A. & Moule, M. (1966). Br. med. J. i, 396.CrossRefGoogle Scholar
Coates, M. E. (1968). In The Vitamins Vol. 2, 2nd ed., p. 212 [Sebrell, W. H. and Harris, R. S, editors’. New York: Academic Press.CrossRefGoogle Scholar
Coates, M. E., Ford, J. E., Harrison, G. F., Kon, S. K. & Porter, J. W. G. (1953). Br. J. Nutr. 7, 319.CrossRefGoogle Scholar
Dawbarn, M. C., Hine, D. C. & Smith, J. (1958). Aust. J. exp. Biol. med. Sci. 36, 541.CrossRefGoogle Scholar
Ellis, F. R. & Montegriffo, V. M. E. (1970). Am. J. clin. Nutr. 23, 249.CrossRefGoogle Scholar
Gompertz, D., Jones, J. H. & Knowles, J. P. (1967). Clinica chim. Acta 18, 197.CrossRefGoogle Scholar
Gräsbeck, R., Nyberg, W. & Reizenstein, P. (1958). Proc. Soc. exp. Biol. Med. 97, 780.CrossRefGoogle Scholar
Gurnani, S., Mistry, S. P. & Johnson, B. C. (1960). Biochim. biophys. Acta 38, 187.CrossRefGoogle Scholar
Gutteridge, J. M. C. & Wright, E. B. (1970). Clinica chim. Acta 27, 289.CrossRefGoogle Scholar
Halstead, J. A., Carroll, J. & Rubert, S. (1959). New Engl. J. Med. 260, 575.CrossRefGoogle Scholar
Herbert, V. & Zalusky, R. (1962). J. clin. Invest. 41, 1263.CrossRefGoogle Scholar
Hogue, D. E. & Elliot, J. M. (1964). J. Nutr. 83, 171.CrossRefGoogle Scholar
Joske, R. A. (1963). Gut 4, 231.CrossRefGoogle Scholar
Kohn, J., Mollin, D. L. & Rosenbach, L. M. (1961). J. clin. Path. 14, 345.CrossRefGoogle Scholar
Mathews, D. M. (1962). Clin. Sci. 22, 101.Google Scholar
Mehta, B. M., Rege, D. V. & Satoskar, R. S. (1964). Am. J. clin. Nutr. 15, 77.CrossRefGoogle Scholar
Mickelsen, O. (1956). Vitams Horm. 14, 1.CrossRefGoogle Scholar
Mollin, D. L., Booth, C. C. & Baker, S. J. (1957). Br. J. Haemat. 3, 412.CrossRefGoogle Scholar
Oace, S. M. & Abbott, J. M. (1972). J. Nutr. 102, 17.CrossRefGoogle Scholar
Oxnard, C. E. & Smith, W. T. (1966). Nature, Lond. 210, 507.CrossRefGoogle Scholar
Powell, D. E. B., Thomas, J. H., Mandal, A. R. & Dignam, C. T. (1969). J. clin. Path. 22, 672.CrossRefGoogle Scholar
Sakami, W. & Ukstins, I. (1961). J. biol. Chem. 236, PC50.CrossRefGoogle Scholar
Seriver, C. R. (1970). Pediatrics, Springfield 46, 493.CrossRefGoogle Scholar
Skeggs, H., Nepple, H. M., Valentik, K. A., Huff, J. W. & Wright, L. D. (1950). J. biol. Chem. 184, 211.CrossRefGoogle Scholar
Smith, A. D. M. (1962). Br. med. J. i, 1655.CrossRefGoogle Scholar
Spray, G. H. (1955). Clin. Sci. 14, 661.Google Scholar
Stewart, J. S., Roberts, P. D. & Hoffbrand, A. V. (1970). Lancet ii, 542.CrossRefGoogle Scholar
Stokstad, E. L. R. (1968). Vitams Horm. 26, 443.CrossRefGoogle Scholar
Thenen, S. W. & Stokstad, E. L. R. (1973). J. Nutr. 103, 363.CrossRefGoogle Scholar
Waters, A. H. & Mollin, D. L. (1961). J. clin. Path. 14, 335.CrossRefGoogle Scholar
Williams, D. L., Spray, G. H., Newman, G. E. & O'Brien, J. R. P. (1969). Br, J. Nutr. 23, 343.CrossRefGoogle Scholar