Abstract
Vitamin E has eight different naturally occurring forms: four tocopherols and four tocotrienols. Because α-tocopherol has three asymmetric carbons, both natural α-tocopherol (RRR-α-tocopherol) and synthetic α-tocopherol (all-rac-α-tocopherol) are utilized in both pharmaceutical products and food additives. Therefore, determining the distribution of vitamin E in the body is very important. With regard to absorption, and transportation of vitamin E, it is suggested that the pathways mediated by three proteins (CD36, SR-BI, and NPC1L1) as well as passive diffusion affect absorption of vitamin E. Vitamin E homologs are mainly transported by very low-density lipoprotein (VLDL) with the α-tocopherol being recognized by the α-tocopherol transfer protein in liver. However, it is also suggested that chylomicrons (CMs) and high-density lipoprotein (HDL) are involved in transportation of vitamin E homologs from the small intestine to each section of peripheral tissue. In particular, it is speculated that vitamin E homologs transportation by CMs and HDL from enterocytes to peripheral tissues such as adipose tissue greatly affects the distribution of vitamin E homologs, excluding α-tocopherol. However, how lipoprotein lipase affects the incorporation of vitamin E homologs containing lipoprotein into peripheral tissues is unclear. Whether there is biodiscrimination when vitamin E homologs are incorporated into peripheral tissues from lipoprotein is an interesting question. It is likely that future research will reveal how individual vitamin E homologs are incorporated into peripheral tissue, especially the brain, adipose tissue, and skin.