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Postprandial Vitamin E Plasma Enrichment and Second Meal Effect in Women with and without Metabolic
Pierre-Christian Violet1, Thom Greene2, Stephanie Teng2
1Molecular and Clinical Nutrition Section, Intramural Research Program, National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK), National Institutes of Health (NIH), Bethesda, MD, United States.
Background:
The effect of meal fat sequence and excess body fat on postprandial changes in vitamin E absorption is unclear.
Objectives:
We investigated postprandial changes in plasma vitamin E enrichment in response to varied dietary fat sequences in healthy women and excess body and liver fat in women with obesity and metabolic dysfunction-associated steatotic liver disease (MASLD).
Methods:
Vitamin E [α-tocopherol (α-T)] pharmacokinetics were assessed using deuterium (d)-labeled α-T administered orally [d3-RRR-α-tocopherol (d3-α-T)] and intravenously [d6-RRR-α-tocopherol (d6-α-T)]. A total of 13 healthy women received oral and intravenous (IV) α-T (30 mg) with a liquid breakfast containing 40% or 0% fat, followed by 30% fat lunch and dinner at 4 h and 8 h, or a 12-h fast (0% fat-fast). A total of 6 women with MASLD and 10 normal weight controls received oral and IV α-T (2 mg) with similar meal sequence. Major outcomes were postprandial plasma α-T %enrichment, maximal concentration (Cmax), and area under the curves (AUCs) at 4, 12, and 24 h. Exploratory outcomes included the second meal effect (SME), defined as mean change in pre-2nd meal compared with post-2nd meal d3-α-T %enrichment at 4 h and 12 h, respectively.
Results:
At 4-h oral d3-α-T %enrichment, Cmax and AUC0-4 h were not statistically different between 40% and 0% fat groups. Following the 2nd meal at 4 h, SME was 55% higher in the 0% group than in the 40% group (15.8% ± 1.1% compared with 10.2% ± 1.1%, P < 0.009), resulting in greater Cmax and AUC in the 0% group at 12 and 24 h (P < 0.04). Compared with the 0% group, the 0% fat-fast group showed reduced oral d3-α-T %enrichment, whereas no differences were seen with IV d6-α-T %enrichments. Compared with controls, the obese/MASLD cohort had 31% lower SME (0.87% ± 0.1% compared with 1.26% ± 0.1%, P = 0.047), resulting in reduced Cmax and AUC (P < 0.04) at 24 h.
Conclusions:
The variation in the meal fat sequence (0%-30% compared with 40%-30% fat) significantly enhanced SME and postprandial d3-α-T %enrichment, whereas obesity/MASLD attenuated SME and postprandial vitamin E %enrichment.
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