Reina Sofía University Hospital, Instituto Maimónides de Investigación Biomédica de Córdoba (IMIBIC), University of Córdoba, Córdoba, Spain.
J Nutr. 2010 Sep;140(9):1595-601. doi: 10.3945/jn.109.120816. Epub 2010 Jul 14.
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.
饮食中的脂肪摄入量对代谢综合征(MetS)的发展起着关键作用。本研究旨在验证这样一个假设,即饮食中的脂肪数量和质量可能会以不同的方式调节 MetS 患者的餐后脂蛋白代谢。在 LIPGENE 研究中进行的一项多中心、平行、随机、对照试验将 MetS 患者随机分配到 4 种饮食组之一:高饱和脂肪酸(HSFA;脂肪提供 38%的能量(E),16%的 E 为 SFA)、高单不饱和脂肪酸(HMUFA;脂肪提供 38%的能量(E),20%的 E 为 MUFA)和 2 种低脂肪、高复合碳水化合物(LFHCC;脂肪提供 28%的能量(E))饮食,同时补充 1.24 克/天的长链(LC)(n-3)PUFA(二十碳五烯酸:二十二碳六烯酸比例为 1.4:1)或安慰剂(1.24 克/天的高油酸葵花籽油),持续 12 周。在干预前后进行了相同脂肪组成的脂肪挑战。在干预前后,测定了餐后总胆固醇、甘油三酯(TG)、载脂蛋白(apo)B、apo B-48、apo A-I、LDL-胆固醇、HDL-胆固醇和胆固醇、甘油三酯、视黄醇棕榈酸和甘油三酯富含脂蛋白(TRL;大、小)中的 apo B。与 HSFA 和 LFHCC 组相比,HMUFA 组餐后 TG(P < 0.001)和大 TRL-TG(P = 0.009)清除开始更早,速度更快。与其他饮食组相比,LFHCC(n-3)组的餐后 TG 浓度更低(P < 0.001)。摄入 LFHCC 饮食会增加餐后 TG(P = 0.04)、大 TRL-TG(P = 0.01)、TRL-胆固醇(P < 0.001)、TRL-视黄醇棕榈酸(P = 0.001)和 TRL-apo B(P = 0.002)的曲线下面积与干预前的值相比。相比之下,长期摄入 LFHCC(n-3)饮食并没有增加餐后 TG 和 TRL 的代谢。总之,代谢综合征相关的餐后异常可以通过 LFHCC(n-3)和 HMUFA 饮食来减轻。通过对体重稳定的 MetS 患者进行 LC(n-3)PUFA 补充,可以避免长期 LFHCC 饮食引起的不良餐后 TG 升高效应。