PNP, PLP, and PMP are enzymatically hydrolyzed in the small intestine to PN, PL, and PM prior to absorption. The intestinal absorption of dietary vitamin B6, in the form of PN, PL, and pM, has historically been ascribed to passive diffusion.181 Recent evidence suggests that a carrier-mediated process may also be involved.182 One additional form of vitamin B6, pyridoxine-5'-j6-D-glucoside (Fig. 28.35), is the predominate form in some plants (grains, fruits, and vegetables), and this form has a significantly lower bioavailabil-ity than other forms because of incomplete hydrolysis of the glycosidic bond in the intestines.
In the liver, all three forms are interconverted; however, the major form of vitamin B6 in the liver is PLP.181 PLP (60%), PN (15%), and PL (14%) circulate in the blood bound to albumin. Vitamin B6 traverses cell membranes, upon entry or exit, only in the dephosphorylated form. Plasma alkaline phosphatase (EC 188.8.131.52) is responsible for the removal of the phosphate group prior to cellular uptake from the blood.183 Upon cellular entry via facilitated transport, phosphorylation acts to trap the vitamin and drive the overall process of cellular uptake.184 Total body stores of vitamin B6 approximate 170 mg with 75% to 80% found in muscle, primarily as phosphorylase (EC 184.108.40.206), and 5% to 10% in the liver185 with the remaining portion distributed among the remaining tissues. The muscle pool is thought to be very stable, relatively unavailable to other tissues and highly conserved during deficient intake. Therefore, deficiency of this vitamin is more likely to affect tissues other than muscle, especially newly formed tis-sues.185 Excess vitamin B6 is eventually converted to PL, which is oxidized to 4-pyridoxic acid. This acid is the primary form found in the urine, accounting for essentially all excess dietary vitamin B6.
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