Corl B A, Butler S T, Butler W R, Bauman D E
Department of Dairy Science, Virginia Polytechnic Institute and State University, Blacksburg 24061, USA.
J Dairy Sci. 2006 Nov;89(11):4172-5. doi: 10.3168/jds.S0022-0302(06)72462-6.
Diet-induced milk fat depression in dairy cows has been known for many years and several theories have been proposed. One that continues to receive support is the glucogenic-insulin theory. Previous studies testing this theory using a hyperinsulinemic-euglycemic clamp have had variable results attributable to variability in the use of body fat reserves as a source of milk fatty acids. Our objective was to test the glucogenic-insulin theory using cows immediately postpartum, a period when the use of body fat for milk fat synthesis is greatest. During wk 2 postpartum, 5 cows were given a 2-d baseline period and then clamped for 4 d. Insulin was increased more than 2-fold during the clamp while the blood glucose concentration was maintained. Milk yield was not altered by administration of the clamp (38.7 vs. 39.0 +/- 1.4 kg/d); however, the milk fat percentage and yield were reduced by 27% and plasma nonesterified fatty acids were reduced by 68%. Analysis of the milk fatty acid composition revealed that the decrease in milk fat yield during use of the clamp was almost exclusively due to reductions in preformed fatty acids; this is the exact opposite of what is observed with diet-induced milk fat depression. Therefore, our results do not support the glucogenic-insulin theory of diet-induced milk fat depression. The results further indicated that reductions in milk fat observed previously with hyperinsulinemic-euglycemic clamps or with glucose or propionate infusions were most likely consequences of the ability of insulin to inhibit lipolysis, thereby limiting the mammary availability of preformed fatty acids mobilized from body reserves.
奶牛因饮食导致乳脂降低的现象已为人所知多年,并且已经提出了几种理论。其中一个仍得到支持的理论是生糖-胰岛素理论。先前使用高胰岛素-正常血糖钳夹法对该理论进行测试的研究结果各不相同,这归因于将体脂储备用作乳脂肪酸来源时的变异性。我们的目标是在产后立即使用奶牛来测试生糖-胰岛素理论,这一时期利用体脂进行乳脂合成的情况最为显著。在产后第2周,5周,给5头奶牛设定了一个为期2天的基线期,然后进行4天的钳夹。在钳夹期间,胰岛素增加了两倍多,同时血糖浓度保持不变。钳夹处理并未改变产奶量(38.7对39.0 +/- 1.4千克/天);然而,乳脂百分比和产量降低了27%,血浆非酯化脂肪酸降低了68%。对乳脂肪酸组成的分析表明,钳夹期间乳脂产量的下降几乎完全是由于预制脂肪酸的减少;这与饮食诱导的乳脂降低所观察到的情况正好相反。因此,我们的结果不支持饮食诱导的乳脂降低的生糖-胰岛素理论。结果还进一步表明,先前使用高胰岛素-正常血糖钳夹法或输注葡萄糖或丙酸盐时观察到的乳脂降低,很可能是胰岛素抑制脂肪分解能力的结果,从而限制了从体储备中动员的预制脂肪酸向乳腺的供应。