(n-3) fatty acid supplementation in moderately hypertriglyceridemic adultschanges postprandial lipid and apolipoprotein B responses to a standardized test meal

Citation
Lf. Tinker et al., (n-3) fatty acid supplementation in moderately hypertriglyceridemic adultschanges postprandial lipid and apolipoprotein B responses to a standardized test meal, J NUTR, 129(6), 1999, pp. 1126-1134
Citations number
58
Categorie Soggetti
Food Science/Nutrition","Endocrinology, Nutrition & Metabolism
Journal title
JOURNAL OF NUTRITION
ISSN journal
00223166 → ACNP
Volume
129
Issue
6
Year of publication
1999
Pages
1126 - 1134
Database
ISI
SICI code
0022-3166(199906)129:6<1126:(FASIM>2.0.ZU;2-J
Abstract
The effects of (n-3) fatty acids on the postprandial state were investigate d by monitoring the alimentary responses to identical test meals fed to adu lts [n = 11; fasting triacylglycerol (TG) 2.55 +/- 0.24 mmol/L; mean +/- SE M] after a self-selected diet baseline period (BLP) and then after a 6-wk ( n-3) fatty acid period (FOP) [similar to 5.2 g (n-3) fatty acids] and a 6-w k control oil period (COP) administered in random order, Samples were drawn immediately prior to the test meal (time 0) and then hourly from 2 to 6 h postmeal. Postprandial plasma triacylglycerol (TG) and TO-rich lipoprotein (TRL) TG apo B48, and B100 absolute concentrations were significantly lower after FOP than after COP or BLP, while plasma cholesterol was unchanged. N ormalizing the results as increments over time 0 eliminated the diet effect on all but plasma TG, Time remained a significant effect for plasma TG, TR L TG, and TRL TC. Finally, only absolute TRL B48 and absolute and increment al plasma TG concentrations displayed significant time-diet interactions. T hese results suggest that postprandial TRL apo B reductions are likely caus ed by (n-3) fatty acid suppression of both hepatic and intestinal apoB secr etion/synthesis, Altered TRL metabolism, i.e. changes in postprandial TG, c holesterol, apo B48, and increase in LDL particle size, may represent an ad ditional mechanism for the reduced heart disease risk associated with fish [(n-3) fatty acid] consumption.