Journal of Nutrition

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Journal of Nutrition Vol. 102 No. 4 April 1972, pp. 571-582
Copyright © 1972 by American Society for Nutrition
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Relation of Riboflavin Deficiency to Corticosteroid Metabolism and Red Cell Hypoplasia in Baboons

Henry Foy, Athena Kondi and Zulfikarali H. M. Verjee

Wellcome Trust Research Laboratories, P.O. Box 30141, Nairobi, Kenya

Riboflavin deficiency was produced by feeding baboons a balanced artificial diet lacking only riboflavin. In the deprived animals structural and functional changes occurred in the adrenal cortex. These changes were accompanied by an erythroid hypoplasia similar to that seen in African children with marasmus and kwashiorkor during the recovery syndrome, and responded to parenteral riboflavin or oral prednisone in both children and baboons. The adrenal cortex in the deprived hypoplastic baboons was hemorrhagic and fibrotic. The 24-hour urinary 17-hydroxycorticosteroid and 17-oxosteroid in the riboflavin-deficient baboons were low when compared with pair-fed baboons and those on a natural diet. Terminally the plasma 11-hydroxycorticosteroids were raised, perhaps related to the high transcortin levels. ACTH stimulation in the riboflavin-deprived animals gave very low or no response, whereas in the pair-fed and natural diet animals the increase was eightfold in the urinary steroids and between 35 and 50% in the plasma steroids. The effect that riboflavin deficiency has on the physiological and morphological state of the adrenal cortex is discussed in relation to marrow activity. Severe skin lesions occurred in all the riboflavin-deprived baboons which responded rapidly and completely to riboflavin but not to prednisone.


KEY WORDS: • riboflavin • corticosteroids • erythroid hypoplasia • baboon

Manuscript received 23 February 1971.


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Riboflavin (vitamin B-2) and health
Am. J. Clinical Nutrition, June 1, 2003; 77(6): 1352 - 1360.
[Abstract] [Full Text] [PDF]




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