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Riboflavin deficiency led to a reduction in the percentage of the <jats:sup>59<\/jats:sup>Fe dose absorbed and an increased rate of <jats:sup>59<\/jats:sup>Fe loss. All post-absorption <jats:sup>59<\/jats:sup>Fe loss could be accounted for by faecal <jats:sup>59<\/jats:sup>Fe, confirming that the loss was gastrointestinal. Fe concentrations and <jats:sup>59<\/jats:sup>Fe as a percentage of retained whole-body <jats:sup>59<\/jats:sup>Fe were higher in the small intestine of riboflavin-deficient animals than their controls, 14 d after the test meal. A separate experiment demonstrated that riboflavin deficiency was associated with a significant proliferative response of the duodenal crypts of the small intestine. 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