Ballou M A, Cruz G D, Pittroff W, Keisler D H, DePeters E J
Department of Animal Science and Nutritional Biology Graduate Group, University of California, Davis 95616, USA.
J Dairy Sci. 2008 Sep;91(9):3478-87. doi: 10.3168/jds.2008-1016.
Fifty-one Jersey bull calves (5 +/- 1 d old) were assigned to 1 of 3 milk replacers to determine the effects of increasing doses of n-3 fatty acids from fish oil on the acute phase response after an endotoxin challenge. All calves were fed a 22.5% crude protein and 18% lipid milk replacer (Calva Products, Acampo, CA) supplemented with an additional 2% fatty acids. Treatments differed only in the supplemental lipid source and included a 3:1 mix of corn and canola oils, a 1:1 blend of fish oil (Omega Proteins, Houston, TX) and the 3:1 mix of corn and canola oils, and fish oil only. On d 23, each calf was injected subcutaneously with 4 microg/kg of body weight of Salmonella Typhimurium endotoxin. Clinical, hematological, and biochemical parameters were measured at 0, 1, 2, 3, 4, 5, 6, 8, 10, 12, 15, 18, 24, and 72 h post endotoxin challenge. Endotoxin caused a dramatic rise in respiratory rate; feeding fish oil significantly attenuated the increase. Heart rate and rectal temperature were not affected by treatment. Feeding fish oil attenuated the change in serum iron concentration over time. Endotoxin caused severe hypoglycemia, reaching a nadir at 4 h. Calves supplemented with fish oil had reduced concentrations of serum glucose for 8 to 24 h. Furthermore, calves supplemented with fish oil alone had reduced serum insulin at 12, 28, and 24 h. In contrast, endotoxin caused an acute increase in blood urea nitrogen and nonesterified fatty acids; there were significant linear effects of fish oil on both blood urea nitrogen and nonesterified fatty acids. Serum triglycerides were elevated beginning at 12 h after the endotoxin challenge and returned to baseline values within 72 h. Fish oil suppressed the rise in triglycerides during this period, and the effect was linear with increasing fish oil. Serum concentrations of leptin decreased after the endotoxin challenge; however, the treatment did not influence the response. There was no treatment effect on serum aspartate aminotransferase or lactate dehydrogenase activity. Adding fish oil to milk replacer attenuated many aspects of the acute phase response, and the effect was linear in the range of 5 to 10% of the lipid replaced as fatty acids from fish oil. Adding fish oil might provide a better balance between a necessary versus an excessive acute phase response.
51头泽西公牛犊(5±1日龄)被分配至3种代乳品中的一种,以确定鱼油中n-3脂肪酸剂量增加对脂多糖攻击后急性期反应的影响。所有犊牛均饲喂含22.5%粗蛋白和18%脂肪的代乳品(Calva Products,阿坎波,加利福尼亚州),并额外添加2%脂肪酸。处理组仅在补充脂肪来源上有所不同,包括玉米油和菜籽油3:1的混合物、鱼油(Omega Proteins,休斯顿,德克萨斯州)与玉米油和菜籽油3:1混合物1:1的混合,以及仅含鱼油。在第23天,每头犊牛皮下注射4μg/kg体重的鼠伤寒沙门氏菌脂多糖。在脂多糖攻击后0、1、2、3、4、5、6、8、10、12、15、18、24和72小时测量临床、血液学和生化参数。脂多糖导致呼吸频率急剧上升;饲喂鱼油显著减轻了这种上升。心率和直肠温度不受处理影响。饲喂鱼油减弱了血清铁浓度随时间的变化。脂多糖导致严重低血糖,在4小时达到最低点。补充鱼油的犊牛在8至24小时内血清葡萄糖浓度降低。此外,仅补充鱼油的犊牛在12、28和24小时血清胰岛素降低。相比之下,脂多糖导致血尿素氮和非酯化脂肪酸急性增加;鱼油对血尿素氮和非酯化脂肪酸均有显著的线性影响。脂多糖攻击后12小时开始血清甘油三酯升高,并在72小时内恢复至基线值。在此期间,鱼油抑制了甘油三酯的升高,且该作用随鱼油增加呈线性。脂多糖攻击后血清瘦素浓度降低;然而,处理未影响该反应。对血清天冬氨酸转氨酶或乳酸脱氢酶活性无处理效应。在代乳品中添加鱼油减轻了急性期反应的许多方面,且在作为脂肪酸从鱼油替代脂质的5%至10%范围内该作用呈线性。添加鱼油可能在必要的急性期反应与过度的急性期反应之间提供更好的平衡。