Apart from milk and eggs, which contain relatively large amounts of free riboflavin bound to specific binding proteins, most of the vitamin in foods is as flavin coenzymes bound to enzymes, which are released when the protein is hydrolyzed. Intestinal phosphatases then hydrolyze the coenzymes to liber-ate riboflavin, which is absorbed in the upper small intestine. The absorption of riboflavin is limited and after moderately high doses only a small proportion is absorbed.
Much of the absorbed riboflavin is phosphorylated in the intestinal mucosa and enters the bloodstream as riboflavin phosphate, although this does not seem to be essential for absorption of the vitamin.
About 50% of plasma riboflavin is free riboflavin, which is the main transport form, with 44% as flavin adenine dinucleotide (FAD) and the remainder as riboflavin phosphate. The vitamin is largely protein-bound in plasma; free riboflavin binds to both albumin and α- and β-globulins; both riboflavin and the coenzymes also bind to immunoglobulins.
Uptake into tissues is by passive carrier-mediated transport of free riboflavin, followed by metabolic trapping by phosphorylation to riboflavin phosphate, and onward metabolism to FAD.
Riboflavin phosphate and FAD that are not bound to proteins are rapidly hydrolyzed to riboflavin, which diffuses out of tissues into the bloodstream. Ribofla-vin and riboflavin phosphate that are not bound to plasma proteins are filtered at the glomerulus; renal tubular resorption is saturated at normal plasma con-centrations. There is also active tubular secretion of the vitamin; urinary excretion of riboflavin after moderately high doses can be two- to threefold greater than the glomerular filtration rate.
Under normal conditions about 25% of the urinary excretion of riboflavin is as the unchanged vitamin, with a small amount as glycosides of riboflavin and its metabolites.
There is no significant storage of riboflavin; apart from the limitation on absorption, any surplus intake is excreted rapidly, so that once metabolic requirements have been met urinary excretion of riboflavin and its metabolites reflects intake until intestinal absorption is saturated. In depleted animals, the maximum growth response is achieved with intakes that give about 75% saturation of tissues, and the intake to achieve tissue saturation is that at which there is quantitative excretion of the vitamin.
There is very efficient conservation of riboflavin in deficiency, and almost the only loss from tissues will be the small amount that is covalently bound to enzymes and cannot be salvaged for reuse. There is only a fourfold difference between the minimum con-centration of flavins in the liver in deficiency and the level at which saturation occurs. In the central nervous system there is only a 35% difference between defi-ciency and saturation.
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