Toral P G, Hervás G, Frutos P
Instituto de Ganadería de Montaña (CSIC-ULE), Finca Marzanas s/n, 24346 Grulleros, León, Spain.
Instituto de Ganadería de Montaña (CSIC-ULE), Finca Marzanas s/n, 24346 Grulleros, León, Spain.
J Dairy Sci. 2015 Mar;98(3):1961-71. doi: 10.3168/jds.2014-8731. Epub 2014 Dec 26.
Oral administration of cobalt has been proven to alter milk fatty acid (FA) composition consistent with an inhibition of mammary stearoyl-coenzyme A desaturase (SCD) activity in ruminants, but the mechanisms explaining its mode of action remain uncertain. In this study, Co (as Co-acetate) was dosed to lactating ewes with the aims of examining mammary gene expression during Co-induced changes in milk FA composition, and estimating the endogenous synthesis of SCD products in milk of sheep fed an 18:3n-3-enriched diet. Twelve Assaf ewes fed a diet supplemented with 2% linseed oil were allocated to 2 experimental groups and received an oral drench supplying either 0 (control) or 9 mg of Co/kg of body weight per day. Treatments were administered in 3 equal doses at 8-h intervals for 6 d. No effects of Co administration on animal performance were observed. The changes in milk FA (namely, reductions in most cis-9-containing FA) were consistent with an inhibition of SCD in the absence of detectable effects on the relative importance of mammary de novo synthesis and FA uptake. The high proportion of endogenous cis-9 trans-11 18:2 observed in this study (89%) would agree with a greater supply of trans-11 18:1 of ruminal origin in ewes fed linseed oil, compared with previous estimates in sheep fed a diet without lipid supplementation. Differences between studies could also be related to diet-induced changes in SCD activity. Altogether, both mechanisms would support that basal diet composition is a major determinant of the relative contribution of Δ9-desaturation to milk FA profile. Similarly, the consumption of a diet rich in 18:3n-3 might also explain the low proportion of milk cis-9 18:1 estimated to derive from Δ9-desaturation (29%). The administration of Co to ewes fed linseed oil allowed to discriminate minor 18:3 isomers in milk, such as cis-9 trans-12 cis-15 18:3, as SCD products. Finally, Co dosing lowered the mRNA abundance of SCD1 in the mammary secretory tissue (33%), whereas no changes were detected in the SCD5 isoform or in the studied transcription factors (SREBF1, PPARG, SP1, and EGR2). These results suggest that the mode of action of Co in dairy ewes would be at least partly mediated by the downregulation of SCD1.
已证实，反刍动物口服钴会改变乳脂肪酸（FA）组成，这与乳腺硬脂酰辅酶A去饱和酶（SCD）活性受到抑制一致，但其作用机制仍不明确。在本研究中，给泌乳母羊投喂钴（以乙酸钴形式），目的是研究钴诱导乳脂肪酸组成变化期间的乳腺基因表达，并估计采食富含18:3n-3日粮的绵羊乳中SCD产物的内源性合成。将12只采食添加2%亚麻籽油日粮的阿萨夫母羊分为2个实验组，分别接受口服灌服，对照组每日每千克体重补充0毫克钴，处理组每日每千克体重补充9毫克钴。处理分3次等量投喂，间隔8小时，持续6天。未观察到钴处理对动物生产性能有影响。乳脂肪酸的变化（即大多数含顺式-9的脂肪酸减少）与SCD受到抑制一致，且未发现对乳腺从头合成和脂肪酸摄取的相对重要性有明显影响。本研究中观察到的内源性顺式-9反式-11 18:2比例较高（89%），这与采食亚麻籽油的母羊瘤胃来源的反式-11 18:1供应量增加一致，与之前采食无脂日粮的绵羊估计值相比有所不同。不同研究之间的差异也可能与日粮诱导的SCD活性变化有关。总之，这两种机制都表明基础日粮组成是Δ9-去饱和作用对乳脂肪酸谱相对贡献的主要决定因素。同样，采食富含18:3n-3的日粮也可能解释了乳中估计源自Δ9-去饱和作用的顺式-9 18:1比例较低（29%）的原因。给采食亚麻籽油的母羊投喂钴能够区分乳中的次要18:3异构体，如顺式-9反式-12顺式-15 18:3，这些异构体是SCD产物。最后，钴处理降低了乳腺分泌组织中SCD1的mRNA丰度（33%），而未检测到SCD5异构体或所研究的转录因子（SREBF1、PPARG、SP1和EGR2）有变化。这些结果表明，钴对泌乳母羊的作用方式至少部分是由SCD1的下调介导的。
