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A Low-Fat, High-Complex Carbohydrate Diet Supplemented with Long-Chain (n-3) Fatty Acids Alters the Postprandial Lipoprotein Profile in Patients with Metabolic Syndrome
Author(s) -
Yolanda Jiménez,
Carmen Marı́n,
Pablo PérezMartínez,
J. Hartwich,
M. MalczewskaMalec,
Iwona Gołąbek,
Beata KiećWilk,
Cristina CruzTeno,
Fernando RodríguezRodríguez,
Purificación Gómez,
Maria J. Gómez-Luna,
Catherine Defoort,
Michael J. Gibney,
Francisco PérezJiménez,
Helen M. Roche,
José LópezMiranda
Publication year - 2010
Publication title -
journal of nutrition
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.463
H-Index - 265
eISSN - 1541-6100
pISSN - 0022-3166
DOI - 10.3945/jn.109.120816
Subject(s) - postprandial , medicine , endocrinology , docosahexaenoic acid , cholesterol , polyunsaturated fatty acid , lipoprotein , carbohydrate , eicosapentaenoic acid , apolipoprotein b , chemistry , fatty acid , biology , biochemistry , insulin
Dietary fat intake plays a critical role in the development of metabolic syndrome (MetS). This study addressed the hypothesis that dietary fat quantity and quality may differentially modulate postprandial lipoprotein metabolism in MetS patients. A multi-center, parallel, randomized, controlled trial conducted within the LIPGENE study randomly assigned MetS patients to 1 of 4 diets: high-SFA [HSFA; 38% energy (E) from fat, 16% E as SFA], high-monounsaturated fatty acid [HMUFA; 38% E from fat, 20% E as MUFA], and 2 low-fat, high-complex carbohydrate [LFHCC; 28% E from fat] diets supplemented with 1.24 g/d of long-chain (LC) (n-3) PUFA (ratio 1.4 eicosapentaenoic acid:1 docosahexaenoic acid) or placebo (1.24 g/d of high-oleic sunflower-seed oil) for 12 wk each. A fat challenge with the same fat composition as the diets was conducted pre- and postintervention. Postprandial total cholesterol, triglycerides (TG), apolipoprotein (apo) B, apo B-48, apo A-I, LDL-cholesterol, HDL-cholesterol and cholesterol, TG, retinyl palmitate, and apo B in TG-rich lipoproteins (TRL; large and small) were determined pre- and postintervention. Postintervention, postprandial TG (P < 0.001) and large TRL-TG (P = 0.009) clearance began earlier and was faster in the HMUFA group compared with the HSFA and LFHCC groups. The LFHCC (n-3) group had a lower postprandial TG concentration (P < 0.001) than the other diet groups. Consuming the LFHCC diet increased the TG (P = 0.04), large TRL-TG (P = 0.01), TRL-cholesterol (P < 0.001), TRL-retinyl palmitate (P = 0.001), and TRL-apo B (P = 0.002) area under the curve compared with preintervention values. In contrast, long-term ingestion of the LFHCC (n-3) diet did not augment postprandial TG and TRL metabolism. In conclusion, postprandial abnormalities associated with MetS can be attenuated with LFHCC (n-3) and HMUFA diets. The adverse postprandial TG-raising effects of long-term LFHCC diets may be avoided by concomitant LC (n-3) PUFA supplementation to weight-stable MetS patients.

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