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 synthetase, suggesting that much of the increased biotin is used for increased carboxylation reactions. However, there is also an increase in the biotinylation of histones compared with quiescent cells, suggesting that biotin has a role in regulation of the cell cycle (Zempleni and Mock, 2000b, 2001; Stanley et al., 2001; Zempleni et al., 2001).
The few early reports of human biotin deficiency all concerned people who consumed large amounts of uncooked eggs and therefore had a high intake of avidin, which binds biotin and renders it unavailable (Section 11.6). Provision of biotin supplements of between 200 to 1000 ^g per day cured the skinlesions despite continuing the abnormal diet providing large amounts of avidin. Unfortunately, there seems to have been no studies of provision of modest doses of biotin to such patients, and none in which their high intake of uncooked eggs was either not replaced by an equivalent intake of cooked eggs (in which avidin has been denatured by heat and the yolks of which are a good source of biotin) or continued unchanged. Thus, there is no information from these case reports on the amounts of biotin that are required for normal health.
More recently, similar signs of biotin deficiency have been observed in patients receiving total parenteral nutrition for prolonged periods, after major resection of the gut. The signs resolve after the provision of biotin, but again there have been no studies of the amounts of biotin required; intakes have ranged between 60 to 200 ^g per day (Mock et al., 1985).
Biotin deficiency, and the functional deficiency associated with lack of holocarboxylase synthetase (Section 184.108.40.206), or biotinidase (Section 220.127.116.11), causes alopecia (hair loss) and a scaly erythematous dermatitis, especially around the body orifices. The dermatitis is similar to that seen in zinc and essential fatty acid deficiency, and is commonly associated with Candida albicans infection. Histology of the skin shows an absence of sebaceous glands and atrophy of the hair follicles. The dermatitis is because of impaired metabolism of polyunsaturated fatty acids as a result of low activity of acetyl CoA carboxylase (Section 18.104.22.168). In biotin-deficient experimental animals, provision of supplements of long-chain «6 polyunsaturated fatty acids prevents the development of skin lesions (Mock et al., 1988a, 1988b; Mock, 1991).
In biotin-deficient rats, the total fatty acid content of the skin is about one-third of normal, and contains a lower than normal proportion of C16 and C18 saturated and unsaturated fatty acids, and a higher than normal proportion of very long-chain fatty acids (especially C24:1 and C26:1). There are also increased amounts of odd-chain fatty acids (C15:0 to C29:0), reflecting impaired activity of propionyl CoA carboxylase (Section 22.214.171.124) and incorporation of propionyl CoA into fatty acids in competition with acetyl CoA (Proud et al., 1990).
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