Astorg P O, Compoint G
Ann Nutr Aliment. 1979;33(5):659-86.
The mean term effects (16 weeks) of brassidic acid (n-9 trans docosenoic acid) and erucic acid (n-9, cis docosenoic acid) on the lipids and fatty acids of different organs in the rat (plasma, adipose tissue, liver, heart) and compared to those of their C 18 homologues, elaidic and oleic acid, in a 2(3) factorial experiment; the three tested factors are: 1) the chain length of the dietary monoenes (C 22:1 vs. C 18:1), 2) the geometrical configuration of their double bond (trans vs. cis) and 3) the dietary levels (30% vs. 1,7% of dietary fatty acids). Experimental details have been reported previously [Astorg and Levillain, 1979]. With a low supply of linoleic acid, brassidic acid, brassidic acid induces a large increase of plasma triacylglycerols (TG), but this can be caused by a slow fat absorption. However, the plasma contents of cis and trans docosenoic acids do not differ greatly. Both docosenoic acids incorporate more into the lipids of heart and adipose tissue than into liver lipids, and, for each organ, more into TG than into phospholipids (PL). In heart and adipose tissue lipids, the percentage of brassidic acid is lower than that of erucic acid. In these 2 organs and in the liver, linoleic acid subdeficiency decreases the incorporation of both C 22:1 isomers into the lipids. Dietary brassidic acid is readily converted to other trans monoenes, mainly elaidic acid, which incorporates into organ lipids. The extent of this chain-shortening may be greater than that of erucic acid (to oleic acid), and this would explain the lower level of brassidic acid found in organ lipids. Last, dietary trans monoenes (brassidic and elaidic acids) induce, as compared to their cis isomers, slight but visible changes in the profile of (n-9) polyunsaturated fatty acids in organ lipids. These results are discussed and related to the fact that brassidic acid does not seem to have the heart pathogenic potency of erucic acid [see part 1 of this paper, Astorg and Levillain, 1979].
在一项2(3)析因实验中,研究了芥酸(n-9反式二十二碳烯酸)和反油酸(n-9顺式二十二碳烯酸)对大鼠不同器官(血浆、脂肪组织、肝脏、心脏)脂质和脂肪酸的平均长期影响(16周),并将其与它们的C18同系物反油酸和油酸进行比较;三个测试因素分别为:1)膳食单烯的链长(C22:1与C18:1),2)其双键的几何构型(反式与顺式),3)膳食水平(膳食脂肪酸的30%与1.7%)。实验细节先前已有报道[阿斯托格和勒维兰,1979年]。在亚油酸供应不足时,芥酸会导致血浆三酰甘油(TG)大幅增加,但这可能是由于脂肪吸收缓慢所致。然而,顺式和反式二十二碳烯酸的血浆含量差异不大。两种二十二碳烯酸在心脏和脂肪组织脂质中的掺入量均多于肝脏脂质,并且对于每个器官,在TG中的掺入量多于磷脂(PL)。在心脏和脂肪组织脂质中,芥酸的百分比低于反油酸。在这两个器官和肝脏中,亚油酸供应不足会减少两种C22:1异构体在脂质中的掺入。膳食芥酸很容易转化为其他反式单烯,主要是反油酸,后者掺入器官脂质中。这种链缩短的程度可能大于反油酸(转化为油酸),这可以解释在器官脂质中发现的芥酸水平较低的原因。最后,与顺式异构体相比,膳食反式单烯(芥酸和反油酸)会导致器官脂质中(n-9)多不饱和脂肪酸谱发生轻微但明显的变化。对这些结果进行了讨论,并与芥酸似乎没有反油酸的心脏致病潜力这一事实相关联[见本文第1部分,阿斯托格和勒维兰,1979年]。