Han L Q, Pang K, Li H J, Zhu S B, Wang L F, Wang Y B, Yang G Q, Yang G Y
College of Animal Science and Veterinary Medicine, Henan Agricultural University, Zhengzhou, China.
Genet Mol Res. 2012 Sep 17;11(4):4754-64. doi: 10.4238/2012.September.17.2.
The efficacy of conjugated linoleic acid (CLA) in diet supplements for milk fat reduction is well documented in several species. However, the mechanisms by which fatty acids regulate mammary lipogenesis remain largely unknown, especially with regard to gene expression of enzyme and regulators. In this study, 8 Holstein dairy cows in their mid-lactation period were randomly divided into 2 groups. Control cows received a Ca salt of palm oil fatty acid dietary supplement, and those in the CLA group were fed Ca salts of CLA (Ca-CLA), all in a dose of approximately 200 g∙cow(-1)∙day(-1) for 14 days. The milk yield was recorded daily, and protein, lactose, and fat in the milk were quantified every 3 days for 2 weeks. Fatty acids in the milk were analyzed with gas-liquid chromatography. Measurement of messenger RNA levels of the main lipogenic genes of lipoprotein lipase, acetyl-coenzyme A (CoA) carboxylase, fatty acid synthase, stearoyl-CoA desaturase, and transcription factors such as sterol response element binding protein 1 (SREBP1) and peroxisome proliferator-activated receptor γ was performed in biopsy samples of mammary tissue on the last day. The results indicated that dietary Ca-CLA caused a continuous reduction of milk fat (P < 0.01) with no effect on milk yield, milk protein, and lactose. The fatty acid profile in the milk from the CLA group differed from that from controls, and the yield of milk fatty acid decreased (P < 0.01) with Ca-CLA supplementation. The depressed expression of lipogenic genes (lipoprotein lipase, acetyl-CoA carboxylase, fatty acid synthase, and stearoyl-CoA desaturase) demonstrated inhibition of fatty acid de novo synthesis and uptake in the mammary gland of the CLA group. Furthermore, the gene expression of transcription factor SREBP1 was also downregulated (P < 0.01), but peroxisome proliferator-activated receptor γ was unchanged, suggesting that SREBP1 may play a key role in the regulation of lipogenic gene expression in the lactating mammary gland.
共轭亚油酸（CLA）在多种物种的日粮补充剂中降低乳脂的功效已有充分记录。然而，脂肪酸调节乳腺脂肪生成的机制在很大程度上仍不清楚，尤其是在酶和调节因子的基因表达方面。在本研究中，8头处于泌乳中期的荷斯坦奶牛被随机分为2组。对照组奶牛接受棕榈油脂肪酸日粮补充剂的钙盐，CLA组奶牛则饲喂CLA的钙盐（Ca-CLA），剂量均约为200 g∙头⁻¹∙天⁻¹，持续14天。每天记录产奶量，并在2周内每3天对牛奶中的蛋白质、乳糖和脂肪进行定量分析。用气相色谱法分析牛奶中的脂肪酸。在最后一天，对乳腺组织活检样本中脂蛋白脂肪酶、乙酰辅酶A（CoA）羧化酶、脂肪酸合酶、硬脂酰-CoA去饱和酶等主要脂肪生成基因以及转录因子如固醇调节元件结合蛋白1（SREBP1）和过氧化物酶体增殖物激活受体γ（PPARγ）的信使RNA水平进行测定。结果表明，日粮Ca-CLA使乳脂持续降低（P < 0.01），而对产奶量、乳蛋白和乳糖没有影响。CLA组牛奶中的脂肪酸谱与对照组不同，补充Ca-CLA后乳脂肪酸产量降低（P < 0.01）。脂肪生成基因（脂蛋白脂肪酶、乙酰-CoA羧化酶、脂肪酸合酶和硬脂酰-CoA去饱和酶）表达降低，表明CLA组乳腺中脂肪酸的从头合成和摄取受到抑制。此外，转录因子SREBP1的基因表达也下调（P < 0.01），但过氧化物酶体增殖物激活受体γ未改变，这表明SREBP1可能在泌乳期乳腺脂肪生成基因表达的调节中起关键作用。
