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短期补充低剂量的γ-亚麻酸(GLA)、α-亚麻酸(ALA)或GLA加ALA,并不能显著提高荷兰纯素食者的长链多不饱和脂肪酸ω-3水平。

Short-term supplementation of low-dose gamma-linolenic acid (GLA), alpha-linolenic acid (ALA), or GLA plus ALA does not augment LCP omega 3 status of Dutch vegans to an appreciable extent.

作者信息

Fokkema M R, Brouwer D A, Hasperhoven M B, Martini I A, Muskiet F A

机构信息

Department of Pathology and Laboratory Medicine, Groningen University Hospital, Groningen, The Netherlands.

出版信息

Prostaglandins Leukot Essent Fatty Acids. 2000 Nov;63(5):287-92. doi: 10.1054/plef.2000.0216.

DOI:10.1054/plef.2000.0216
PMID:11090255
Abstract

Vegans do not consume meat and fish and have therefore low intakes of long chain polyunsaturated fatty acids (LCP). They may consequently have little negative feedback inhibition from dietary LCP on conversion of alpha -linolenic acid (ALA) to the LCP omega 3 eicosapentaenoic (EPA) and docosahexaenoic (DHA) acids. We investigated whether supplementation of nine apparently healthy vegans with 2.01 g ALA (4 ml linseed oil), 1.17 g gamma-linolenic acid (GLA) (6 ml borage oil) or their combination increases the LCP omega 3 contents of erythrocytes (RBC) and platelets (PLT), and of plasma phospholipids (PL), cholesterol esters (CE) and triglycerides (TG). The supplements changed the dietary LA/ALA ratio (in g/g) from about 13.7 (baseline) to 6.8 (linseed oil), 14.3 (borage oil) and 6.4 (linseed + borage oil), respectively. ALA or GLA given as single supplements did not increase LCP omega 3 status, but their combination augmented LCP omega 3 (in CE) and EPA (in fasting TG) to a statistically significant, but nevertheless negligible, extent. We conclude that negative feedback inhibition by dietary LCP, if any, does not play an important role in the inability to augment notably DHA status by dietary ALA. The reach of a DHA plateau already at low dietary ALA intakes suggests that dietary DHA causes a non-functional DHA surplus, or is, alternatively, important for maintaining DHA status at a functionally relevant level.

摘要

纯素食者不吃肉类和鱼类,因此长链多不饱和脂肪酸(LCP)的摄入量较低。因此,他们可能很少受到膳食LCP对α-亚麻酸(ALA)转化为LCPω-3二十碳五烯酸(EPA)和二十二碳六烯酸(DHA)的负反馈抑制。我们研究了给九名明显健康的纯素食者补充2.01克ALA(4毫升亚麻籽油)、1.17克γ-亚麻酸(GLA)(6毫升琉璃苣油)或它们的组合,是否会增加红细胞(RBC)、血小板(PLT)以及血浆磷脂(PL)、胆固醇酯(CE)和甘油三酯(TG)中LCPω-3的含量。这些补充剂分别将膳食中LA/ALA的比例(以克/克计)从约13.7(基线)改变为6.8(亚麻籽油)、14.3(琉璃苣油)和6.4(亚麻籽+琉璃苣油)。单独补充ALA或GLA并不会提高LCPω-3的水平,但它们的组合在一定程度上提高了LCPω-3(在CE中)和EPA(在空腹TG中),达到了统计学上显著但仍然微不足道的程度。我们得出结论,膳食LCP的负反馈抑制(如果存在的话)在无法通过膳食ALA显著提高DHA水平方面并不起重要作用。在膳食ALA摄入量较低时就已达到DHA平台期,这表明膳食DHA会导致无功能的DHA过剩,或者对将DHA水平维持在功能相关水平很重要。

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