Utliization of Riboflavin
Little is known about the mechanism of intestinal sorption of riboflavin from normal levels of dietary intake in humans. Absorption of doses from has been found to be much greater when the avin is ingested with food than when given on an empity stomach. Bile also appears to stimulate riboflavin absovation . Phosphorylated forms of riboflavin are dephosphorylated prior to the mucosal uptake and resphorylated with in the cell. Active absorption against concentration gradient has been demonstrated in the from low luminal concentrations of the vitamin, but not from high concentrations.
Most of the tissue riboflavin is found in flavoproteins as FAD and the remainder as FMN and free riboflavin. FMN is an intermediate in the synthesis of FAD. On low riboflavin intakes the tissues appear to conserve FAD at the expense of the other forms, and very little riboflavin is excreted in the urine. The tissues have a limited capacity to retain riboflavin and on increasing intakes, urinary excretion of riboflavin increases. The level of urinary excretion of riboflavin is used as a measure of riboflavin status. However, negative nitrogen balance due to insufficient protein intake or other causes is associated with increased loss of riboflavin in the urine and can result in erroneous interpretation of excretion data.
Utilization of riboflavin and, accordingly, riboflavin status, also are influenced by hormones. Both thyroid and adrenal hormones are known to affect the conversion of riboflavin to its coenzyme forms.The use of oral contraceptive agents (OCA) is associated with an increased frequency of marginal riboflavin status in women oflow socioeconomic status, but no effects have been observed in presumably well-nourishednourishedOCAusers.Biochemical evidence of riboflavin deficiency has been found in newborn infants with hyperbilirubinemia who are treated with phototherapy.Because it is light-sensitive, riboflavin is presumed to decompose during the treatment.
