Waldron M R, Kulick A E, Bell A W, Overton T R
Department of Animal Science, Cornell University, Ithaca, NY 14853, USA.
J Dairy Sci. 2006 Feb;89(2):596-610. doi: 10.3168/jds.S0022-0302(06)72123-3.
Twenty Holstein cows in early lactation (7 d in milk) were administered 100 microg of Escherichia coli lipopolysaccharide (LPS) dissolved in 10 mL of sterile 0.9% NaCl saline (treatment; TRT) or 10 mL of sterile saline (control) into both right mammary quarters to test the hypothesis that acute experimental mastitis would have negative impacts on aspects of energy metabolism that might lead to the development of metabolic disorders. A primed continuous intravenous infusion (14-micromol/kg of BW priming dose; 11.5-micromol/kg of BW per h continuous infusion) of 6,6-dideuterated glucose was used to determine pre- and posttreatment glucose kinetics using steady-state tracer methodologies. The LPS-treated cows displayed productive, clinical, and physiological signs of moderate to severe inflammation; control cows displayed no signs of immune activation. Pretreatment glucose rates of appearance (Ra) into plasma were similar (715 and 662 +/- 33 mmol/h for TRT and control, respectively) between treatment groups. Intramammary LPS infusion into TRT cows resulted in increased glucose Ra relative to control cows (mean glucose Ra from 150 through 270 min after intramammary infusion were 815 and 674 +/- 21 mmol/h for TRT and control cows, respectively). Furthermore, plasma concentrations of glucose increased, whereas plasma nonesterified fatty acids, glycerol, and beta-hydroxybutyrate concentrations decreased, in TRT relative to control cows. Interestingly, plasma insulin concentration increased dramatically in TRT cows and occurred prior to the small increase in plasma glucose concentration. Although these results only represent the early stages of inflammation, they are not consistent with a causal relationship between mastitis and energy-related metabolic disorders and instead suggest a coordinated protective effect by the immune system on metabolism during the early stages of mammary insult.
选用20头处于泌乳早期(产犊后7天)的荷斯坦奶牛,分别向其右乳区注入溶解于10 mL无菌0.9%氯化钠生理盐水的100微克大肠杆菌脂多糖(LPS)(处理组;TRT)或10 mL无菌生理盐水(对照组),以验证急性实验性乳腺炎会对能量代谢方面产生负面影响从而可能导致代谢紊乱这一假设。采用初量连续静脉输注(14微摩尔/千克体重的初量;11.5微摩尔/千克体重每小时连续输注)6,6 - 二氘代葡萄糖,运用稳态示踪方法测定处理前后的葡萄糖动力学。LPS处理的奶牛表现出中度至重度炎症的生产、临床和生理体征;对照奶牛未表现出免疫激活迹象。处理组之间,处理前血浆葡萄糖的出现率(Ra)相似(TRT组和对照组分别为715和662±33毫摩尔/小时)。相对于对照奶牛,向TRT组奶牛乳腺内注入LPS导致葡萄糖Ra增加(乳腺内注入后150至270分钟的平均葡萄糖Ra,TRT组和对照组奶牛分别为815和674±21毫摩尔/小时)。此外,相对于对照奶牛,TRT组奶牛的血浆葡萄糖浓度升高,而血浆非酯化脂肪酸、甘油和β - 羟基丁酸浓度降低。有趣的是,TRT组奶牛的血浆胰岛素浓度急剧增加,且发生在血浆葡萄糖浓度略有升高之前。尽管这些结果仅代表炎症的早期阶段,但它们并不支持乳腺炎与能量相关代谢紊乱之间的因果关系,反而表明在乳腺损伤早期免疫系统对代谢具有协同保护作用。