Animal and Avian Sciences Department, University of Maryland, College Park 20742.
Department of Ruminant Science, Institute of Animal Sciences, Volcani Center, Bet Dagan 50250, Israel.
J Dairy Sci. 2013 Apr;96(4):2387-2399. doi: 10.3168/jds.2012-5861. Epub 2013 Feb 15.
During diet-induced milk fat depression (MFD), the short and medium-chain fatty acids (SMCFA), which are synthesized de novo in the mammary gland, are reduced to a much greater extent than the long-chain fatty acids (LCFA) that originate from the circulation. Our hypothesis was that increased availability of SMCFA might rescue conjugated linoleic acid (CLA)-induced MFD in lactating dairy cows. To test that hypothesis, 4 rumen-fistulated lactating Holstein cows (128 ± 23 d in milk) were used in a 4 × 4 Latin square design with 3-wk experimental periods. Treatments were applied during the last 2 wk of each period and included 3× daily abomasal infusion of a total of (1) 230 g/d of LCFA (blend of 59% cocoa butter, 36% olive oil, and 5% palm oil); (2) 420 g/d of butterfat (BF); (3) 230 g/d of LCFA with 27 g/d of CLA (LC-CLA), containing 10 g/d of trans-10,cis-12 CLA; and (4) 420 g/d of butterfat with 27 g/d of CLA (BF-CLA). Butterfat provided 50% of C16 (115 g/d) and similar amounts of C18 FA as found in LCFA, such that the difference between the BF and LCFA treatments was 190 g/d of SMCFA. No treatment effects were observed for DMI or milk yield. Milk fat content was reduced by 41 and 32%, whereas milk fat yield was reduced by 41 and 38% with LC-CLA and BF-CLA, respectively, compared with their respective controls. Abomasal infusion of CLA reduced de novo synthesized fatty acid (DNFA; SMCFA and 50% C16:0) concentration, whereas DNFA tended to be greater with BF infusion. An interaction was observed between SMCFA and CLA as the increased availability of SMCFA reduced stearoyl-CoA-desaturase-1 gene expression, whereas it tended to reduce lipoprotein lipase (LPL), 1-acylglycerol-3-phosphate O-acyltransferase 6 (AGPAT-6), sterol regulatory element-binding protein cleavage-activating protein (SCAP), and peroxisome proliferator-activated receptor γ (PPAR-γ) gene expression in the presence of CLA. The mRNA expression of genes involved in de novo fatty acid synthesis [acetyl-coenzyme A carboxylase α (ACACA) and fatty acid synthase (FASN)], fatty acid uptake (LPL), and triglyceride synthesis [AGPAT-6 and diacylglycerol O-acyltransferase 1 (DGAT-1)] along with protein abundance of the ACC and FASN were reduced with CLA. However, the increased availability of SMCFA had no effect on lipogenic gene expression except for LPL, whose expression was increased with BF infusion. The nutritional manipulation by increasing the intestinal availability of SMCFA was not sufficient to rescue CLA-induced MFD.
在饮食诱导的乳脂降低(MFD)期间,短链和中链脂肪酸(SMCFA)的合成在乳腺中从头合成,其减少程度远大于源自循环的长链脂肪酸(LCFA)。我们的假设是,增加 SMCFA 的可利用性可能会挽救共轭亚油酸(CLA)诱导的泌乳奶牛的 MFD。为了验证这一假设,我们使用了 4 头瘤胃瘘管泌乳荷斯坦奶牛(泌乳 128 ± 23 天),采用 4×4 拉丁方设计,每个实验期 3 周。在每个周期的最后 2 周内应用处理,包括(1)每天 3 次胃灌注共 230 g/d 的 LCFA(59%可可脂、36%橄榄油和 5%棕榈油的混合物);(2)420 g/d 的乳脂;(3)230 g/d 的 LCFA 加 27 g/d 的 CLA(LC-CLA),其中含有 10 g/d 的反式-10,顺式-12 CLA;和(4)420 g/d 的乳脂加 27 g/d 的 CLA(BF-CLA)。乳脂提供 115 g/d 的 C16(50%)和与 LCFA 中发现的相似量的 C18 FA,使得 BF 和 LCFA 处理之间的差异为 190 g/d 的 SMCFA。DMI 或产奶量没有观察到处理效果。乳脂含量分别降低了 41%和 32%,而 LC-CLA 和 BF-CLA 分别降低了 41%和 38%的乳脂产量。CLA 的胃灌注降低了从头合成脂肪酸(DNFA;SMCFA 和 50% C16:0)的浓度,而 BF 灌注时 DNFA 趋于增加。观察到 SMCFA 和 CLA 之间存在相互作用,因为 SMCFA 的可用性增加降低了硬脂酰辅酶 A 去饱和酶-1 基因的表达,而在存在 CLA 时,它倾向于降低脂蛋白脂肪酶(LPL)、1-酰基甘油-3-磷酸 O-酰基转移酶 6(AGPAT-6)、固醇调节元件结合蛋白切割激活蛋白(SCAP)和过氧化物酶体增殖物激活受体 γ(PPAR-γ)基因的表达。参与从头脂肪酸合成的基因[乙酰辅酶 A 羧化酶 α(ACACA)和脂肪酸合酶(FASN)]、脂肪酸摄取(LPL)和甘油三酯合成[AGPAT-6 和二酰基甘油 O-酰基转移酶 1(DGAT-1)]的 mRNA 表达以及 ACC 和 FASN 的蛋白丰度随着 CLA 的增加而降低。然而,增加 SMCFA 的可利用性除了 LPL 外,对脂肪生成基因表达没有影响,LPL 的表达随着 BF 灌注而增加。通过增加肠道中 SMCFA 的可利用性进行的营养操作不足以挽救 CLA 诱导的 MFD。