Biotin renal transport

Biotin is essential for cell proliferation. Peripheral blood mononuclear cells appear to take up biotin by a system that is distinct from the sodium-dependent multivitamin transporter that is responsible for intestinal and renal uptake of biotin (Section 11.1). In response to mitogenic stimuli the uptake of biotin increases several-fold, with no change in the activity of the sodium-dependent transporter. At the same time, there is an increase in the rate of expression of methylcrotonyl CoA, propionyl CoA carboxylases, and holocarboxylase... 

The anticonvulsants primidone and carbamazepine inhibit biotin uptake into brush-border membrane vesicles from human intestine (Zempleni et al. 2009). Long-term therapy with anticonvulsants increases both biotin catabolism and urinary excretion of 3-hydroxyisovaleric acid. These eifects might be due to displacement of biotin from biotinidase by anticonvulsants, thereby aifecting plasma transport, renal handling or cellular uptake of biotin. 

The relationship of these putative biotin transporters to each other and their relative roles in intestinal absorption, transport into various organs, and renal reclamation remain to be elucidated. 

Animal studies and studies using brush border membrane vesicles from human kidney cortex indicate that biotin is reclaimed from the glomerular filtrate against a concentration gradient by a saturable, Na -depen-dent, structurally specific system, but biocytin does not inhibit tubular reabsorption of biotin. Subsequent egress of biotin from the tubular cells occurs via a basolateral membrane transport system that is not dependent on Na. Studies of patients with biotinidase deficiency surest that there may be a role for biotinidase in the renal handling of biotin. 

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