TABLE 5.

AUC_{0–8 h} derived from plasma lipoprotein d₃- and d₆-α-tocopherol enrichment percentages¹

Lipoprotein	40% fat	0% fat	0% fat-fast	Intervention, P value	Lipoprotein, P value	Interaction, P value
d6-α-T AUC0–8 h (% · h)
IV dose
TRL2	160 ± 13	171 ± 8	174 ± 13	0.7145	0.0183*	0.4964
LDL3	158 ± 13	167 ± 8	171 ± 13
HDL	154 ± 13	162 ± 8	169 ± 13
d3-α-T AUC0–8 h (% · h)
Oral dose
TRL2	82 ± 13	62 ± 5	34 ± 5	0.0022*	<0.0001*	0.2926
LDL3	28 ± 13	34 ± 5	12 ± 5
HDL	30 ± 13	34 ± 5	12 ± 5

¹AUC_{0–8 h} (% · h, mean ± SEM) calculated from the lipoprotein d₃- and d₆-α-tocopherol enrichment percentages from 0 to 8 h following oral d₃- and IV d₆-α-tocopherol administration to women consuming different fat levels during the defined liquid meal [40% fat, n = 7 (lipoproteins were not obtained for subjects 1–3); 0% fat, n = 10; 0% fat, fasting 12 h, n = 7]. To determine the α-T disposition into the lipoprotein fractions, a Latin square design with double repeated measures (Kronecker product) in SAS PROC MIXED was used independently for each route (oral compared with IV) of α-T administration. Fixed effects were the intervention (40% fat, 0% fat, 0% fat-fast), the lipoprotein fractions (TRL, LDL, HDL), and their interaction. The variance–covariance structure within subjects was modeled by using a Kronecker product in which the treatment was modeled using a compound symmetry matrix, and the lipoprotein fractions within treatment were modeled using an unstructured variance–covariance matrix. *Statistically significant values. IV, intravenous.

²TRL, density <1.006 g/L.

³LDL, 1.006 < density > 1.063 g/mL.