Absorption, dietary biotin

Most dietary biotin is bound to protein, the amide linkage being broken prior to absorption. At least eight children have been described who have multiple carboxylase deficiency with low activities of several of the biotin-requiring carboxylases, i.e., multiple carboxylase deficiency (Table 38-1). Pharmacological doses of biotin restored the activities of the carboxylases in these patients, indicating that the defect was not in the apocarboxylases. Thus, the defect is presumably in the intestinal transport system, in holocarboxylase synthetase, or in some step in cellular uptake or intracellular transport of biotin. 

Contrary to its free form, dietary biotin is not ready for intestinal absorption. For this reason, its bio availability can vary from 5% to close to 100% depending on foodstulfs ingested (Said et al. 1993). 

Free biotin is subsequently released by the action of another and specific enzyme, namely biotinidase. The latter step is critical as it conditions efficient absorption and optimal bioavailability of dietary biotin. The carboxyl group of the valeric acid moiety of the biotin molecule must be free for its recognition by the involved transport mechanism through the intestinal enterocytes (Said and Redha 1987). Intestinal biotinidase is found in pancreatic juice, secretion of the intestinal glands, bacterial flora and the brush-border membranes. 

Pantothenic acid is taken in as dietary CoA compounds and dCphosphopantetheine and hydrolyzed by pyrophosphatase and phosphatase in the intestinal lumen to dephospho-CoA, phosphopantetheine, and pantetheine. This is further hydrolyzed to pantethenic acid. The vitamin is primarily absorbed as pantothenic acid by a saturable process at low concentrations and by simple diffusion at higher ones. The saturable process is facilitated by a sodium-dependent multivitamin transporter, for which biotin and lipoate compete. After absorption, pantothenic acid enters the circulation and is taken up by cells in a manner similar to its intestinal adsorption. The synthesis of CoA from pantothenate is regulated by pantothenate kinase, which itself is subject to negative feedback from the products CoA and acyi-CoA. The steps involved were outlined above. Pantothenic acid is excreted in the urine after hydrolysis of CoA compounds by enzymes that cleave phosphate and the cys-teamine moieties. Only a small fraction of pantothenate is secreted into milk and even less into colostrum. 

Dietary Reference intakes. These have been difficult to determine. There has been some speculation that humans might obtain part of their biotin requirements from the intestinal flora in the colon. The question that has not been adequately answered is whether there is significant absorption of bacteria-pro-duced biotin from the colon. 

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