Blood flow and nutrient exchange across the liver and gut of the dairy cow

Blood flow and nutrient exchange across the liver and gut of the dairy cow
复制标题

奶牛肝脏和肠道的血流和营养物质交换

DOI:
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发表时间:
1983
影响因子:
3.6
通讯作者:
G. D. Baird
G. D. Baird
中科院分区:
医学3区
文献类型:
--
作者:
M. Lomax;G. D. Baird

文献摘要

被引文献

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1.测定了哺乳期和非哺乳期奶牛(A)在正常饲喂状态和(B)禁食前、中、后6d的门静脉和肝静脉血流速度,以及肠道和肝脏的挥发性脂肪酸(VFA)、葡萄糖、乳酸、丙酮酸、氨基酸、酮体、甘油、非酯化脂肪酸(NEFA)和氧气的净交换。2.正常、哺乳、哺乳奶牛的肝脏血流速度比非哺乳奶牛高52%,禁食后两组奶牛的肝脏血流速度均降低。门脉血流量随着代谢能(ME)摄入量的增加而增加。3.与非哺乳期相比,哺乳期奶牛的动脉血葡萄糖和乳酸浓度较低,门静脉VFA和酮体净输出量较高,肝脏葡萄糖净输出量较高,丙酸和乳酸的肝脏净摄入量较高。泌乳奶牛内脏中的醋酸盐、葡萄糖和羟丁酸的产量均明显高于对照组。4.禁食引起血中VFA浓度迅速下降,甘油和NEFA浓度升高。门脉(即肠道)、VFA、乳酸、酮体、丙氨酸和(丝氨酸+苏氨酸)的输出量以及门脉对O2的摄取均在禁食后下降。禁食6h后,肝脏葡萄糖和乙酸酯的排出量分别减少77%和95%,丙酮酸、甘油和NEFA的摄取量增加,酮体排出量增加一倍。禁食还降低内脏乙酸盐和葡萄糖的产量以及内脏对O2的摄取量。5.饲喂和禁食奶牛的门静脉VFA、乳酸和羟丁酸净输出量以及肝脏葡萄糖净输出量均与能量摄入量呈正相关。肝脏葡萄糖输出量也与产奶量相关。6.本研究中测量的肝脏对糖异生前体的净摄取量可以解释禁食奶牛的肝脏净葡萄糖输出量,但不能解释喂食奶牛的净肝脏葡萄糖输出。肝脏对生酮前体丁酸盐和NEFA的净摄取足以解释饲喂和禁食奶牛的酮体的肝脏输出,但肝脏对生酮前体的摄取不太可能也解释观察到的醋酸酯的肝脏输出。
1. The rate of blood flow in the portal and hepatic veins, and the net exchange across the gut and liver of volatile fatty acids (VFA), glucose, lactate, pyruvate, amino acids, ketone bodies, glycerol, non-esterified fatty acids (NEFA) and oxygen, were measured in lactating and non-lactating cows (a) in the normal, fed state and (b) before, during and after 6 d of fasting. 2. Blood flow rate through the liver was 52% higher in normal, fed, lactating cows as compared with non-lactating cows, and was decreased by fasting in both groups of cows. Portal blood flow rate increased with an increase in metabolizable energy (ME) intake. 3. Lactating, as compared with non-lactating, cows exhibited lower arterial concentrations of glucose and lactate, higher net portal outputs of VFA and ketone bodies, a higher net hepatic output of glucose, and higher net hepatic uptakes of propionate and lactate. The splanchnic outputs of acetate, glucose and hydroxybutyrate were all apparently greater in the lactating cows. 4. Fasting caused a rapid decrease in the blood concentrations of the VFA and an increase in those of glycerol and NEFA. The portal, i.e. gut, outputs of VFA, lactate, ketone bodies, alanine and (serine+threonine), and the portal uptake of O2, were all decreased by fasting. Fasting for 6 h also decreased the hepatic output of glucose and acetate by 77 and 95% respectively, increased the hepatic uptake of pyruvate, glycerol and NEFA, and doubled hepatic ketone-body output. The splanchnic output of acetate and glucose and the splanchnic uptake of O2 were also decreased by fasting. 5. The net portal outputs of VFA, lactate and hydroxybutyrate, and the net hepatic output of glucose, were all correlated with ME intake in fed and fasted cows. Hepatic glucose output was also correlated with milk yield. 6. The net hepatic uptake of gluconeogenic precursors measured in this study could account for net hepatic glucose output in the fasted cows, but not in the fed cows. The net hepatic uptake of the ketogenic precursors butyrate and NEFA was sufficient to account for the hepatic output of ketone bodies in both fed and fasted cows, but it is unlikely that the hepatic uptake of ketogenic precursors could also account for the observed hepatic output of acetate.