The human diet contains the range of vitamin E types, with y-tocopherol as the most abundant form in the typical American diet (2). Despite the higher y-tocopherol intake, its concentration in human plasma is 5-10 times less than that of a-tocopherol. Administration of 250 mg a-, y-, or S-tocotrienol/d for 8 wk did not lead to plasma levels >1 ^mol/L (3). It is generally believed that all forms of vitamin E are equally absorbed in the intestine [for review see (4)] and that the preferential treatment of a-tocopherol occurs in the liver by means of the a-tocopherol transfer protein (a-TTP; see below). Studies with children with cholestatic liver disease (5) and with patients suffering from cystic fibrosis (6) demonstrated that uptake of vitamin E into intestinal mucosa cells requires bile acids and pancreatic enzymes. Absorption is believed to be a passive process facilitated by fat intake. Release of vitamin E into the circulation occurs via chylomicrons. The mechanism of chylomicron formation and lipid loading is relatively well known (7), whereas it remains unclear how chylomicrons are loaded with different forms of vitamin E. In cultured hepatocytes, fibroblasts, and macrophages, an a-TTP-dependent but lipoprotein assembly-independent process was reported (8). Similar to the cholesterol reverse transport, it appears to be mediated by the ABCA1 transporter (9). Whether such a pathway is also functioning in the intestine requires investigation.

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