Chelikani Prasanth K, Glimm David R, Keisler Duane H, Kennelly John J
Department of Agricultural, Food and Nutritional Science, University of Alberta, Edmonton, AB, Canada T6G 2P5.
J Dairy Res. 2004 Aug;71(3):288-96. doi: 10.1017/s0022029904000299.
We determined the relative importance of cholecystokinin (CCK), leptin, and fatty acid concentrations in plasma in mediating the satiety effects of supplemental fat in lactating cows. Five ruminally and duodenally cannulated Holstein cows in late lactation were used in a 3 x 5 incomplete Latin square design with three treatments: 1) CONTROL: basal diet (CON), 2) CONTROL+supplementation of canola oil at 1 kg/d in the feed (FED) and 3) CONTROL+abomasal infusion of canola oil at 1 kg/d (INF). Relative to CON, feed intake was reduced by INF but not by FED. We provide evidence that both FED and INF treatments stimulated CCK gene expression in the duodenum and elevated plasma CCK concentrations. However, our results did not support a role for CCK in mediating satiety through an endocrine mechanism of action. We speculate that CCK might be acting either through paracrine and/or neurocrine routes to influence feed intake in cattle. Both FED and INF had no effect on the mRNA abundance of leptin, lipoprotein lipase, or acetyl-CoA carboxylase in adipose tissue. Plasma concentrations of leptin, insulin and IGF-I were not altered by FED or INF, indicating that these signals may not be involved in mediating short-term hypophagic effects of dietary fat. Plasma concentrations of 18:1n-9 and 18:2n-6 were significantly greater for INF than for FED or CON. We conclude that the hypophagic effects of supplemental fat in cattle depend on the amount of unsaturated fatty acids reaching the intestine and that this satiety effect is mediated through CCK, oleic acid and (or) linoleic acid, but leptin is not involved.
我们确定了血浆中胆囊收缩素（CCK）、瘦素和脂肪酸浓度在介导泌乳奶牛补充脂肪的饱腹感效应中的相对重要性。选用5头处于泌乳后期、瘤胃和十二指肠插管的荷斯坦奶牛，采用3×5不完全拉丁方设计，设三种处理：1）对照：基础日粮（CON）；2）对照+在饲料中每天补充1千克菜籽油（FED）；3）对照+每天向真胃灌注1千克菜籽油（INF）。与CON相比，INF组采食量降低，但FED组未降低。我们提供的证据表明，FED和INF处理均刺激十二指肠中CCK基因表达并提高血浆CCK浓度。然而，我们的结果不支持CCK通过内分泌作用机制介导饱腹感。我们推测CCK可能通过旁分泌和/或神经分泌途径影响牛的采食量。FED和INF对脂肪组织中瘦素、脂蛋白脂肪酶或乙酰辅酶A羧化酶的mRNA丰度均无影响。FED或INF未改变血浆中瘦素、胰岛素和IGF-I的浓度，表明这些信号可能不参与介导日粮脂肪的短期摄食减少效应。INF组血浆中18:1n-9和18:2n-6的浓度显著高于FED组或CON组。我们得出结论，牛补充脂肪的摄食减少效应取决于到达肠道的不饱和脂肪酸量，这种饱腹感效应是通过CCK、油酸和（或）亚油酸介导的，但与瘦素无关。
