biotin in the small intestine and prevent its absorption (Mock, 1996).
Biotinidase is thought to play a critical role in the release of biotin from covalent binding to protein (Wolf et al., 1984). Doses of free (unbound) biotin in the range of the estimated typical dietary intake (50 to 150 µg/day) given to individuals who have biotinidase deficiency have been shown to prevent the symptoms seen in biotinidase deficiency, indicating that biotinidase deficiency results in a relative biotin deficiency through lack of adequate digestion of protein-bound biotin, inadequate renal reabsorption, or both.
A biotin carrier located in the intestinal brush border membrane transports biotin against a sodium ion concentration gradient and is structurally specific, temperature dependent, and electroneutral; at pharmacological concentrations, diffusion predominates (Mock, 1996).
Biotin is synthesized by intestinal microflora (Bonjour, 1991). Although transporter-mediated absorption of biotin is most active in the proximal small intestine of the rat, significant absorption of biotin from the proximal colon occurs, which gives credence to the concept that biotin from microbial synthesis within the colon can contribute to meeting the human requirement. From reports of increased blood concentrations after colonic instillation of biotin, it appears that biotin is absorbed from the human colon (Innis and Allardyce, 1983; Oppel, 1948; Sorrell et al., 1971). However, Kopinski and colleagues (1989a, b) have shown that biotin synthesized by enteric flora may not be present at a location or in a form that contributes importantly to absorbed biotin.
The mechanism of biotin transport to the liver and other tissues after absorption has not been well established (Mock, 1996). Biotinidase has been identified as possibly serving as a biotin-binding protein in plasma or as a transporter protein to assist biotin’s entry into the cell (Chauhan and Dakshinamurti, 1988; Wolf et al., 1985). Other studies suggest that serum biotin is more than 80 percent unbound (Hu et al., 1994; Mock and Malik, 1992; Schenker et al., 1993). An acid anion carrier with relative specificity for biotin resembling the intestinal carrier appears to mediate uptake by liver cells (Bowers-Komro and McCormick, 1985). Placental uptake of