Wei Ziang, Guo Yuanyin, Zhang Yi, Cao Jie
College of Veterinary Medicine, China Agricultural University, Beijing 100193, China.
College of Animal Science and Technology, China Agricultural University, Beijing 100193, China.
ACS Omega. 2024 Nov 13;9(47):47042-47051. doi: 10.1021/acsomega.4c07014. eCollection 2024 Nov 26.
Conjugated linoleic acid (CLA) can regulate fatty acid metabolism and increase the content of unsaturated fatty acids in milk during the nutritional regulation process in dairy cows. However, its effects on milk composition and milk energy output in dairy cows remain unclear. We aimed to investigate whether RP-CLA reduces milk energy output during early lactation while lowering milk fat, as well as whether it affects milk protein synthesis and the potential mechanisms. We examined the milk composition of Holstein fresh cows at different stages by administering RP-CLA for 7 days and analyzing related gene expression in the MAC-T cell line. RP-CLA did not significantly alter milk yield, lactose, or blood ketone levels in early lactation. Starting RP-CLA from day 21 postpartum reduced milk fat by about 26% (3.74% vs 2.78%) on day 28 postpartum, slightly increased milk protein, and improved blood glucose on day 24. No such effects were seen with RP-CLA beginning on day 7 postpartum. RP-CLA supplementation saved 6.45 and 11.43% milk energy output during days 7-14 and 21-28, respectively. We hypothesize that the limited RP-CLA regulation effect during days 7-21 may relate to intense lipid mobilization under negative energy balance. In MAC-T cells under low glucose, t-10, c-12 CLA decreased the expression of and , while increased , indicating its role in reducing fat synthesis, easing energy deficiency, promoting cell proliferation, and enhancing protein synthesis. Similarly, under normal glucose, t-10, c-12 CLA suppressed SREBP1 and elevated expression, with reduction only at low doses. Inhibiting milk fat synthesis with an SREBP1 inhibitor slightly upregulated without significantly affecting . In conclusion, RP-CLA has the potential to alleviate negative energy balance in dairy cows during days 21-35 postpartum. t10, c12 CLA can inhibit milk fat synthesis by reducing the expression of SREBP1 and AMPK in mammary epithelial cells, while increasing the expression of CDK1, thereby improving the cellular energy status and promoting milk protein synthesis. The energy required for the increase in milk protein is not derived from the energy saved by the inhibition of milk fat synthesis by CLA.
共轭亚油酸（CLA）在奶牛营养调控过程中可调节脂肪酸代谢并提高牛奶中不饱和脂肪酸的含量。然而，其对奶牛产奶成分和产奶能量输出的影响仍不明确。我们旨在研究反刍动物共轭亚油酸（RP-CLA）是否会在降低乳脂的同时减少泌乳早期的产奶能量输出，以及它是否会影响乳蛋白合成及其潜在机制。我们通过对荷斯坦初产奶牛连续7天给予RP-CLA并分析MAC-T细胞系中的相关基因表达，来检测不同阶段的牛奶成分。RP-CLA在泌乳早期并未显著改变产奶量、乳糖或血酮水平。产后第21天开始使用RP-CLA可使产后第28天的乳脂降低约26%（3.74%对2.78%），略微增加乳蛋白，并在第24天改善血糖。产后第7天开始使用RP-CLA则未观察到此类效果。补充RP-CLA在第7 - 14天和第21 - 28天分别节省了6.45%和11.43%的产奶能量输出。我们推测在第7 - 21天期间RP-CLA有限的调节作用可能与负能量平衡下强烈的脂质动员有关。在低糖条件下的MAC-T细胞中，t-10，c-12 CLA降低了 和 的表达，同时增加了 的表达，表明其在减少脂肪合成、缓解能量不足、促进细胞增殖和增强蛋白质合成方面的作用。同样，在正常葡萄糖条件下，t-10，c-12 CLA抑制了固醇调节元件结合蛋白1（SREBP1）并提高了 的表达，仅在低剂量时 有所降低。用SREBP1抑制剂抑制乳脂合成可略微上调 ，但对 无显著影响。总之，RP-CLA有潜力缓解产后第21 - 35天奶牛的负能量平衡。t10，c12 CLA可通过降低乳腺上皮细胞中SREBP1和AMPK的表达来抑制乳脂合成，同时增加细胞周期蛋白依赖性激酶1（CDK1）的表达，从而改善细胞能量状态并促进乳蛋白合成。乳蛋白增加所需的能量并非来自CLA抑制乳脂合成所节省的能量。
