Instituto de Ganadería de Montaña (CSIC-ULE), Finca Marzanas s/n. 24346 Grulleros, León, Spain.
Instituto de Investigación en Ciencias de la Alimentación (CSIC-UAM), Nicolás Cabrera, 9. Campus de Cantoblanco, 28049 Madrid, Spain.
J Dairy Sci. 2012 Sep;95(9):5242-5252. doi: 10.3168/jds.2012-5349.
This study was conducted in lactating ewes to examine the involvement of ∆(9)-desaturase in mammary lipogenesis, especially in the endogenous synthesis of cis-9, trans-11 18:2 and cis-9 18:1, because no information on this matter was available for dairy sheep. With this aim, 6 Assaf ewes were monitored in a 15-d experiment, which included a 5-d pretreatment period, a 5-d treatment period, and a 5-d posttreatment period. During the treatment period, ewes received 0.5 g/d of sterculic acid (a cyclopropene fatty acid that inhibits ∆(9)-desaturase), delivered intravenously in 4 equal doses at 6-h intervals. Animals were fed pasture to supply mainly α-linolenic acid and minimize the amount of milk cis-9, trans-11 18:2 of ruminal origin. Sterculic acid administration was calculated to inhibit ∆(9)-desaturase by 70% based on the milk content of cis-9 14:1. This inhibition resulted in decreases in the milk content of the enzyme products (e.g., cis-9 10:1, cis-9 14:1, cis-9 16:1, cis-9 18:1, and cis-9, trans-11 18:2) and increases in its substrates (e.g., 14:0, 18:0, and trans-11 18:1), as well as in reductions in the desaturase indexes. Some other milk fatty acids, further to previously reported products or substrates of ∆(9)-desaturase (e.g., cis-15 18:1 and cis-9, cis-15 18:2, or trans-11, trans-15 18:2, and cis-9, trans-11, trans-15 18:3), were also affected by sterculic acid administration. Endogenous synthesis was the major source of cis-9 18:1 and cis-9, trans-11 18:2, accounting for 63 and 74% of its content in milk fat, respectively. To our knowledge, the present study provides the first estimates of endogenous synthesis of these 2 bioactive fatty acids in ovine milk fat.
本研究旨在探讨 ∆(9)-去饱和酶在乳脂生物合成中的作用,特别是在顺式-9, 反式-11 18:2 和顺式-9 18:1 的内源性合成中的作用,因为目前尚无关于奶绵羊的相关信息。为此,我们对 6 只阿萨夫奶绵羊进行了为期 15 天的实验监测,包括 5 天的预处理期、5 天的处理期和 5 天的治疗后恢复期。在处理期内,绵羊每隔 6 小时静脉注射 0.5 克/天的表甾醇酸(一种环丙烯脂肪酸,可抑制 ∆(9)-去饱和酶)。动物被喂食牧场,以提供主要的α-亚麻酸,并最大限度地减少瘤胃来源的牛奶中顺式-9, 反式-11 18:2 的含量。根据牛奶中顺式-9 14:1 的含量,我们计算出甾醇酸的给药量可抑制 ∆(9)-去饱和酶 70%。这种抑制作用导致酶产物(例如顺式-9 10:1、顺式-9 14:1、顺式-9 16:1、顺式-9 18:1 和顺式-9, 反式-11 18:2)的含量降低,其底物(例如 14:0、18:0 和反式-11 18:1)的含量增加,同时去饱和酶指数降低。除了先前报道的 ∆(9)-去饱和酶的产物或底物(例如顺式-15 18:1 和顺式-9, 顺式-15 18:2,或反式-11, 反式-15 18:2 和顺式-9, 反式-11, 反式-15 18:3)外,其他一些牛奶脂肪酸也受到甾醇酸给药的影响。内源性合成是顺式-9 18:1 和顺式-9, 反式-11 18:2 的主要来源,分别占牛奶脂肪中这两种生物活性脂肪酸含量的 63%和 74%。据我们所知,本研究首次估计了这两种生物活性脂肪酸在绵羊乳脂中的内源性合成。