共查询到19条相似文献，搜索用时 718 毫秒
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在4头门静脉、肝静脉、肠系膜静脉和股动脉上安装血管导管的绵羊中研究了克伦特罗（CL,0.8 mg/kgBW,肠系膜静脉给药,每天2次,连续5 d）对其肝脏生长代谢的影响。结果表明:CL对肝脏血流量影响较小。而在CL作用下绵羊血浆中尿素氮水平明显下降,肝静脉和门静脉血液尿素氮流量分别减少16.86％（P<0.01）和15.51％（P<0.05）。肝静脉多肽流量在CL处理期也较对照期下降38.71％（P<0.01）,门静脉处多肽水平处理期则与对照期相当。克伦特罗还增加绵羊肝脏IGF-I的合成和分泌,门静脉和肝静脉中的增加幅度分别为38.84％（P<0.01）和33.18％（P<0.01）。提示CL可通过增强对绵羊肝脏氮的储留及肝脏IGF-I的合成和分泌从而促进机体的生长代谢。 相似文献
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十二指肠灌注不同水平的玉米淀粉对生长肥育绵羊小肠内葡萄糖消化及吸收的影响 总被引：2，自引：0，他引：2
本试验采用4×4的随机区组设计 ,选用5只带有瘤胃、十二指肠近端和回肠末端瘘管的试验羊进行颈动脉、肠系膜静脉、门静脉和肝静脉血管插管的安装 ,并进行十二指肠淀粉灌注试验 ,其中进入十二指肠的淀粉水平分别为33.61g/d、100g/d、150g/d和200g/d(十二指肠淀粉灌注量分别为0、66.39、116.39和166.39g/d)。研究结果表明 :随着十二指肠淀粉灌注水平的提高 ,淀粉在小肠的消化量随之增加 ,而淀粉在小肠的消化率却随之下降 ;绵羊门静脉葡萄糖净流量、肝脏葡萄糖净生成量、肝静脉葡萄糖流量和胰高血糖素/胰岛素比随之提高。但当进入十二指肠的淀粉水平达到150g/d和200g/d时 ,绵羊门静脉葡萄糖净流量、肝脏葡萄糖净生成量、肝静脉的葡萄糖流量和胰高血糖素/胰岛素比出现平台期 ,这表明提高外源性葡萄糖的供应量 ,可促进绵羊门静脉葡萄糖净流量、肝脏葡萄糖净生成量以及肝静脉的葡萄糖流量 ;绵羊小肠对过瘤胃淀粉的消化和吸收的“度”值为150g/d(11.6g/kgW0.75/d)。另外 ,未进行十二指肠淀粉灌注的绵羊门静脉葡萄糖净流量出现负值 ,表明绵羊肠道组织对葡萄糖的消耗量大于被门静脉吸收的葡萄糖量。试验中还发现 ,过瘤胃淀粉在小肠中的消失量 (X)与PDV组织的葡萄糖消耗量 (Y)之间存在显著的相关关系 ,其回归公式 相似文献
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海南霉素是我国生产的第一个聚醚类离子载体抗生素。我们的前期研究表明 ,添喂海南霉素时 ,瘤胃发酵类型发生改变 ,C2/C3 降低。本试验主要进一步研究海南霉素对能量物质吸收、代谢及调节的影响。试验在8头同时装有门静脉、肝静脉、股动脉、股静脉和肠系膜静脉慢性血管瘘的羯山羊(平均体重16.0±2.2kg)上进行 ,按自身对照设计。试验期按0.05mg/kg体重添喂海南霉素。分别测门静脉引流区和肝脏静脉挥发性脂肪酸(VFA)、游离脂肪酸(FFA)、葡萄糖(GS)以及胰岛素和胰高血糖素的净流量。结果显示 ,喂海南霉素使门静脉TVFA和丙酸净流量分别升高24.44 %(3.36vs2.70mmol/min,P<0.05)和84.48 %(1.07vs0.58mmol/min,P<0.05) ,GS和FFA净流量都明显提高(P<0.05)。肝脏乙酸(P<0.05)和丙酸(P<0.01)净流量明显减少 ,GS净流量无明显变化(P>0.05) ,FFA净流量明显降低(P<0.05)。门静脉、肝静脉中胰岛素净流量分别减少66.95 %(11.81vs35.73mU/min)和52.09 %(10.76vs22.64ng/min,P<0.05) ,而胰高血糖素净流量分别比对照期升高50.19 %(19.78vs13.17ng/ml;P>0.05)和307.63 %(4.81vs1.18ng/ml;P<0.05)。结果表明 ,添喂海南霉素能使VFA的吸收量增加 ,促进肝脏中丙酸异生成葡萄糖 ,及乙酸转化成脂肪酸。胰岛素与胰高血糖素的比值(I/ 相似文献
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外源性半胱胺对山羊门静脉和肝脏中激素和营养物流量的影响 总被引：2，自引：0，他引：2
采用6只体重(18.97±1.80)kg、健康雄性去势山羊,同时安装颈静脉、门静脉、肝静脉、肠系膜静脉以及股动脉慢性血管瘘。采用自身对照试验,研究半胱胺对山羊血流量、激素流量和碳氮化合物吸收及在肝脏代谢的影响。试验结果显示,从颈静脉一次注入半胱胺(50 mg/kg BW)后,3 d门静脉、肝静脉全血流量分别比对照(-2d)提高21.81%(P<0.01)、10.21%(P<0.05);血浆流量相应提高23.08%(P<0.05)、15.05%(P<0.05);6 d与-2 d血液流量接近。在-2 d、3 d、6 d 3个采样日,肝脏IGF-1净生成量相应为47.57,67.58(P<0.05)和44.76μg/min;肝脏胰岛素净利用量相应为2.32,3.17和2.23 mU/min,无显著差异;胰高血糖素肝脏净利用量分别为1.71,3.25(P<0.05)和1.02 ng/min。结果表明,从颈静脉注入半胱胺后,肝脏有净乙酸和葡萄糖生成,分别较对照提高12.71%和50.59%(P<0.05);3 d6、d比-2 d在门静脉的NEFA净流量分别提高32.25%和9.67%;肝脏NEFA净流量在试验期3 d和6 d分别比对照提高4.57倍(P<0.01)和4.14倍(P<0.01),表明经CS处理后,山羊肝脏有NEFA合成。门静脉α-氨基氮、NH3-N净流量在第3天分别高于对照36.36%和27.23%,尿素氮净流量也有增高趋势,但差异均未达到显著水平。 相似文献
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添喂海南霉素对山羊肝脏胰岛素样生长因子的影响 总被引：2，自引：0，他引：2
胰岛素样生长因子 -I(IGF -I)是哺乳动物下丘脑—垂体—靶器官生长轴的终端 ,在动物生长过程中起着重要作用。它的浓度变化与生长速度呈正相关。此外 ,它参与泌乳、生殖以及免疫等功能的调节。肝脏具有丰富的生长激素受体 ,是产生IGF -I代谢的主要器官。研究IGF -I在肝脏的产生量及其调节是十分有兴趣的领域。本文根据我室有关“海南霉素能够调节反刍动物瘤胃微生物发酵提高丙酸产生量 ,改善葡萄糖代谢和蛋白质的利用”的研究结果 ,深入观察其对肝脏IGF -I代谢的影响。试验在8头同时装有门静脉、肝静脉、股动脉、股静脉和肠系膜静脉慢性血管瘘的生长羯山羊上进行 ,按自身对照设计。试验期按0.05mg/kg 体重添喂海南霉素 ,分别测门静脉、肝静脉、股动脉、股静脉的血流量和IGF -I的净流量。结果显示 ,试验期山羊门静脉、肝静脉血流量分别比对照期增加15.16 %(1.876vs1.629L/min)和10.80%(2.216vs2.000L/min)。门静脉、肝静脉和股动脉血液中IGF -I含量比对照期分别增加31.5 %(339.8vs258.4ng/ml;P<0.01)、35.83 %(355.6vs261.8ng/ml;P<0.01)和41.08%(352.0vs249.5ng/ml;P<0.01)。对照期和试验期门静脉IGF -I的净流量分别为304.9和485.9ng/min;肝动脉分别为294.4ng/min(P<0.05)和502.7ng/min ;肝静脉分别为40 相似文献
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试验将6头安装永久性瘤胃瘘管以及门静脉、肝静脉以及股动脉慢性血管瘘的泌乳中期中国荷斯坦奶牛随机分为2组,研究不同精粗比日粮对奶牛瘤胃发酵与肝脏VFA代谢以及产奶性能的影响。结果显示:与低精料(LC)日粮组相比,高精料(HC)日粮组瘤胃液pH显著下降(P0.05),丙酸浓度显著提高(P0.05),乙酸/丙酸的比值有降低的趋势(P=0.06),但日粮对瘤胃液乙酸、丁酸和TVFA浓度影响不显著(P0.05)。HC日粮能显著提高门静脉血浆中乙酸、丙酸、丁酸和TVFA(P0.05)浓度。在两种日粮条件下,VFA肝静脉-门静脉血浆浓度差(H-P)均为负值。HC日粮显著增加丙酸和丁酸的H-P值(P0.05)。与LC日粮相比,HC日粮显著增加乙酸和TVFA(P0.05)的肝静脉-动脉血浆浓度差(HA),显著降低丙酸(P0.05)H-A值。HC日粮显著提高门静脉、肝静脉和股动脉血浆中葡萄糖、β-羟丁酸和非酯化脂肪酸(P0.05)浓度以及显著提高乳蛋白、乳中总固形物和非脂固形物(P0.05)含量。试验结果表明,HC日粮可以改善奶牛瘤胃发酵、肝脏的VFA代谢以及生产性能。 相似文献
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添喂海南霉素对山羊肝脏含氮化合物代谢的影响 总被引：1，自引：0，他引：1
肝脏是体内十分主要的代谢器官 ,本试验在有关海南霉素对反刍动物消化代谢的影响研究的基础上 ,进一步探讨添喂海南霉素后对肝脏中含氮化合物代谢的影响。试验在8头同时装有门静脉、肝静脉、股动脉、股静脉和肠系膜静脉慢性血管瘘的羯山羊上进行 ,按自身对照设计。试验期按0.05mg/kg 体重添喂海南霉素 ,分别测门静脉引流区和肝脏中氨氮(NH3-N)、α -氨基氮(α -AAN)和尿素氮(Ure -N)净流量。结果显示 ,添喂海南霉素使肝静脉血流量分别增加15.16 %和10.80 %,门静脉、肝静脉中NH3-N浓度明显降低(P<0.01) ,而α -氨基氮(α -AAN)浓度显著升高(P<0.05)。结果表明 ,海南霉素能够提高山羊门静脉引流区氨基酸的吸收量 ,提高蛋白质的利用效率 相似文献
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《中国畜牧杂志》2016,(21)
本试验旨在研究饲粮粗蛋白质(CP)水平对仔猪门静脉回流组织(PDV)氮代谢的影响规律及机制。试验选用18头出生日龄接近的健康杜×长×大三元杂交猪(20±1.0)kg,分别安装门静脉、颈动脉、肠系膜静脉和肝静脉血插管,采用单因子完全随机设计分配到日粮赖氨酸、蛋氨酸、苏氨酸和色氨酸水平一致而CP水平分别为20.0%(对照)、17.0%和14.0%的3组饲粮中。1周后通过血插管采集血液样品,离心获取血浆,用于分析血浆中排流物质的浓度。结果表明:仔猪门静脉、肝静脉和肝动脉葡萄糖(GLU)浓度不受饲粮CP水平的影响(P0.05),而门静脉GLU的净流量以及肝脏GLU的消耗量皆随饲粮水平的降低而显著降低(P0.01);仔猪肝脏总蛋白(TP)的产量不受饲粮CP水平的影响(P0.05);14.0%CP组仔猪肝脏尿素氮(UN)的产量显著低于对照组(P0.05)。平衡4种重要必需氨基酸的情况下降低饲粮蛋白水平降低了肝脏UN的生成量,但是并未降低肝脏UN生成量与蛋白质采食量的比值。 相似文献
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本试验旨在研究十二指肠灌注大豆小肽对奶山羊小肠小肽和游离氨基酸吸收的影响。选择7只体况良好、体质量相近的奶山羊((37.88±3.03)kg),安装永久性十二指肠近端瘘管和门静脉、肠系膜静脉近端和远端以及颈动脉慢性血插管进行4×4拉丁方试验,分别从十二指肠灌注生理盐水、60、120、180g.d-1大豆小肽。结果表明,随着十二指肠大豆小肽灌注水平的提高,奶山羊肠系膜排流组织(MDV)总肽结合氨基酸净流量显著增加(P0.05或P0.01);60、120、180g.d-1组门静脉排流组织(PDV)总肽结合氨基酸净流量均显著高于对照组(P0.05),但3个大豆小肽灌注组间无显著性差异(P0.05)。奶山羊小肠对小肽的吸收率随小肠中肽量的增加而下降。随着大豆小肽灌注水平的增加,奶山羊MDV和PDV组织游离氨基酸净流量显著增加(P0.05)。随十二指肠大豆小肽灌注水平的提高,试验羊颈静脉血浆尿素氮浓度显著增加(P0.05),对血浆葡萄糖、胰岛素、生长激素、胰高血糖素和IGF-1浓度没有显著影响(P0.05)。研究结果表明,大豆小肽灌注增加奶山羊小肠中肽结合氨基酸的流量,提高了MDV肽结合氨基酸的净流量,但因肽结合氨基酸吸收率降低或/和肽结合氨基酸吸收细胞降解率提高,降低了进入肠系膜静脉的肽结合氨基酸的比率。 相似文献
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Four steers fitted with a ruminal cannula and chronic indwelling catheters in the mesenteric artery, mesenteric vein, hepatic portal vein, hepatic vein, and the right ruminal vein were used to study the absorption and metabolism of VFA from bicarbonate buffers incubated in the temporarily emptied and washed reticulorumen. Portal and hepatic vein blood flows were determined by infusion of p-aminohippurate into the mesenteric vein, and portal VFA fluxes were calibrated by infusion of isovalerate into the ruminal vein. The steers were subjected to four experimental treatments in a Latin square design with four periods within 1 d. The treatments were Control (bicarbonate buffer) and VFA buffers containing 4, 12, or 36 mmol butyrate/kg of buffer, respectively. The acetate content of the buffers was decreased with increasing butyrate to balance the acidity. The butyrate absorption from the rumen was 39, 111, and 300 +/- 4 mmol/h for the three VFA buffers, respectively. The ruminal absorption rates of propionate (260 +/- 12 mmol/h), isobutyrate (11.4 +/- 0.7 mmol/h), and valerate (17.3 +/- 0.7 mmol/h) were not affected by VFA buffers. The portal recovery of butyrate and valerate absorbed from the rumen increased (P < 0.01) with increasing butyrate absorption and reached 52 to 54 +/- 4% with the greatest butyrate absorption. The liver responded to the increased butyrate absorption with a decreasing fractional extraction of propionate and butyrate, and with the greatest butyrate absorption, the splanchnic flux was 22 +/- 1% and 18 +/- 1% of the absorbed propionate and butyrate, respectively. The increased propionate and butyrate release to peripheral tissues was followed by increased (P < 0.05) arterial concentrations of propionate (0.08 +/- 0.01 mmol/kg) and butyrate (0.07 +/- 0.01 mmol/kg). Arterial insulin concentration increased (P = 0.01) with incubation of VFA buffers compared with Control and was numerically greatest with the greatest level of butyrate absorption. We conclude that the capacity to metabolize butyrate by the ruminal epithelium and liver is limited. If butyrate absorption exceeds the metabolic capacity, it affects rumen epithelial and hepatic nutrient metabolism and affects the nutrient supply of peripheral tissues. 相似文献
12.
Four steers fitted with a ruminal cannula and chronic indwelling catheters in the mesenteric artery, mesenteric vein, hepatic portal vein, hepatic vein, and the right ruminal vein were used to study VFA absorption from bicarbonate buffers incubated in the washed reticulorumen, and metabolism by splanchnic tissues. Portal and hepatic vein blood flows were determined by infusion of p-aminohippurate into the mesenteric vein. The steers were subjected to four experimental treatments in a Latin square design. The treatments were Control (ruminal bicarbonate buffer with [mmol/kg]: acetate = 72; propionate = 30; isobutyrate = 2.1; butyrate = 12; valerate = 1.2; caproate = 0; and heptanoate = 0); Val (same as control except for valerate = 8 mmol/kg); Cap (same as control except for caproate = 3.5 mmol/kg); and Hep (same as control except for heptanoate = 3 mmol/kg). All buffers were incubated for 90 min in the rumen, and ruminal VFA absorption rates were maintained by continuous intraruminal infusion of VFA. The arterial concentrations of valerate and heptanoate showed a small increase (< or = 1 micromol/L; P < 0.05) with inclusion of the respective acid in the ruminal buffer, but no change (P = 0.57) in arterial concentration of caproate was detected. Valerate increased (P < 0.05) the net portal flux of butyrate and valerate, as well as the net splanchnic flux of propionate, butyrate, and valerate. With Cap and Hep, the net portal flux of caproate and heptanoate accounted for 54 and 45% of ruminal disappearance rates, respectively, indicating that these acids were extensively metabolized by the ruminal epithelium. Caproate was ketogenic both in the ruminal epithelium and in the liver, and Cap increased (P < 0.05) the arterial concentration, ruminal vein minus arterial concentration difference, net hepatic flux, and net splanchnic flux of 3-hydroxybutyrate. The net hepatic flux of glucose decreased (P = 0.02) with Cap and Hep compared with Control and Val; however, no effect (P = 0.14) on the net splanchnic flux of glucose could be detected. We conclude that the strong biological activity of valerate, caproate, and heptanoate warrant increased emphasis on monitoring their ruminal presence and their potential systemic effects on ruminant metabolism. 相似文献
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瘤胃乙酸、丙酸比例对绵羊体内氧化代谢和血浆胰岛素水平动态变化的影响 总被引：2，自引：0，他引：2
本研究以全胃营养灌注绵羊为试验动物 ,用物质代谢区室分析方法和同位素示踪技术研究了瘤胃乙酸、丙酸比例对体内氧化代谢和血浆胰岛素水平动态变化的影响。不同试验处理间营养灌注液能量、蛋白质水平相同 ,而瘤胃灌注混合挥发性脂肪酸的乙酸、丙酸比例不同。三种混合挥发性脂肪酸的乙酸、丙酸比例分别为75 :15(VFA1)、65 :25(VFA2)、45 :45(VFA3)。由测定引入 14C -乙酸后血液二氧化碳放射比强度—时间曲线上升段斜率(k值)反映体内氧化代谢强度。试验结果为 ,瘤胃灌注VFA1 时的k值显著高于灌注VFA2 和VFA3 时的k值(P<0.05) ,而VFA2 和VFA3 两处理间的差异不显著(P>0.05) ,说明瘤胃灌注VFA1 时绵羊体内氧化代谢强度增加。向停止灌注24小时的绵羊瘤胃内灌注VFA1,血浆胰岛素水平在恢复灌注后缓慢上升。将瘤胃灌注混合挥发性脂肪酸由VFA1 换为VFA2 后 ,血浆胰岛素水平迅速上升 ,之后迅速下降 ,而由VFA2 换为VFA3 后未出现血浆胰岛素水平的明显变化 ,说明血浆胰岛素水平的变化与体内糖代谢调节状态有关 ,而瘤胃灌注VFA1 时的体内糖代谢调节状态与灌注VFA2 和VFA3 时明显不同。 相似文献
14.
Six steers fitted with a ruminal cannula and chronic indwelling catheters in the mesenteric artery, mesenteric vein, hepatic portal vein, hepatic vein, as well as in the right ruminal vein were used to study metabolism of VFA absorbed from buffers in the emptied and washed reticulorumen. [2-(13)C]Acetate was infused into a jugular vein to study portal-drained visceral (PDV) uptake of arterial acetate, hepatic unidirectional uptake of acetate, and whole-body irreversible loss rate (ILR). Isobutyrate was infused into the right ruminal vein to calibrate VFA fluxes measured in the portal vein. On sampling days, the rumen was emptied and incubated in sequence with a 0-buffer (bicarbonate buffer without VFA), a VFA-buffer plus continuous intraruminal infusion of VFA, and finally another 0-buffer. Ruminal VFA absorption was determined as VFA uptake from the VFA-buffer and metabolic effects determined as the difference between metabolite fluxes with VFA-buffer and 0-buffers. Steady absorption rates of VFA were maintained during VFA-buffer incubations (4 h; 592+/-16, 257+/-5, 127+/-2, 17+/-<1, 20+/-<1 mmol/h, respectively, of acetate, propionate, butyrate, isovalerate, and valerate). The portal flux of acetate corrected for PDV uptake of arterial acetate accounted for 105+/-3% of the acetate absorption from the rumen, and the net portal flux of propionate accounted for 91+/-2% of propionate absorption. Considerably less butyrate (27+/-3%) and valerate (30+/-3%) could be accounted for in the portal vein. The sum of portal VFA and 3-hydroxybutyrate as well as lactate represented 99+/-3% of total VFA acetyl units and 103+/-2% of VFA propionyl units. Estimates are maximum because no accounting was made for lactate derived from glycolysis in the PDV. The net splanchnic flux of VFA, lactate, 3-hydroxybutyrate, and glucose accounted for 64+/-2% of VFA acetyl units and 34+/-5% of VFA propionyl units. Results indicate that there is a low "first-pass" uptake of acetate and propionate in the ruminal epithelium of cattle, whereas butyrate and valerate are extensively metabolized, though seemingly not oxidized to carbon dioxide in the epithelium but repackaged into acetate, 3-hydroxybutyrate, and perhaps other metabolites. When PDV "second-pass" uptake of arterial nutrients is accounted for, PDV fluxes of VFA, lactate, and 3-hydroxybutyrate represent VFA production in the gastrointestinal tract and thereby VFA availability to the ruminant animal. 相似文献
15.
本试验旨在研究长期饲喂高精料饲粮下添加复合缓冲剂(碳酸氢钠20 g/d、氧化镁12 g/d、丁酸钠20 g/d)对奶山羊乳成分、血浆生化指标及激素含量的影响。选择8头安装门静脉及肝静脉瘘管处于泌乳中期的奶山羊随机分为2组,分别饲喂基础饲粮(高精料饲粮组,HG组)和基础饲粮+复合缓冲剂(高精料饲粮+复合缓冲剂组,BG组)。预试期为7 d,正试期为143 d。结果显示:与HG组相比,复合缓冲剂显著升高采食后010 h瘤胃液p H平均值(P0.05);复合缓冲剂显著降低肝静脉血浆中非酯化脂肪酸的含量(P0.05),对门静脉和肝静脉血浆中葡萄糖、β-羟丁酸含量无显著影响(P0.05),对肝脏组织中甘油三酯和总蛋白含量无显著影响(P0.05);复合缓冲剂显著降低门静脉血浆中胰岛素和胰高血糖素的含量(P0.05),对门静脉和肝静脉血浆中胰岛素样生长因子1和生长激素的含量无显著影响(P0.05);复合缓冲剂显著或极显著升高产奶量、乳脂率、乳蛋白率、乳非脂固形物率(P0.05或P0.01)。综合得出,在长期高精料饲粮饲喂条件下,由碳酸氢钠、氧化镁、丁酸钠组成的复合缓冲剂能通过影响奶山羊血浆生化指标及激素含量,影响体机营养物质代谢,最终有效提高产乳量与改善乳品质。 相似文献
16.
D L Harmon K L Gross K K Kreikemeier K P Coffey T B Avery J Klindt 《Journal of animal science》1991,69(3):1223-1231
Six Holstein steers (313 +/- 10 kg BW) surgically fitted with hepatic portal, mesenteric venous, mesenteric arterial, and hepatic venous catheters were used in a replicated crossover design experiment to evaluate the feeding of Acremonium coenophialum-infected fescue hay on portal-drained visceral and hepatic nutrient metabolism. Only four steers had functional hepatic catheters. Infected (INF) and endophyte-free (EF) fescue hays were harvested on the same day in May, at the soft dough stage of maturity, from a similar location in southeast Kansas. The hay was chopped through a 2.5-cm screen and fed in 12 portions daily. Intake was limited to 5.2 kg of DM/d to equalize consumption. Each experimental period lasted 21 d. Dietary CP concentration was greater for INF than for EF (9.9 vs 8.6%); however, apparent digestibilities of DM (52.6%) and N (37%) were not different. Ruminal total VFA concentrations and molar proportions were not different with the exception of butyrate, which was increased (P less than .10) for steers when they were fed INF. Feeding of INF increased (P less than .05) arterial beta-hydroxybutyrate concentration and decreased (P less than .10) arterial butyrate concentration. Steers fed EF showed a greater (P less than .05) portal-arterial concentration difference for acetate and an increased (P less than .05) net portal flux of acetate (500 vs 620 mmol/h). No differences in net flux were noted for any of the other VFA, glucose, lactate, urea N, insulin, glucagon, or prolactin.(ABSTRACT TRUNCATED AT 250 WORDS) 相似文献
17.
Effects of increased ammonia and/or arginine absorption on net splanchnic (portal-drained viscera [PDV] plus liver) metabolism of nonnitrogenous nutrients and hormones in cattle were examined. Six Hereford x Angus steers (501 +/- 1 kg BW) prepared with vascular catheters for measurements of net flux across the splanchnic bed were fed a 75% alfalfa:25% (as-fed basis) corn and soybean meal diet (0.523 MJ of ME/[kg BW(0.75).d]) every 2 h without (27.0 g of N/kg of DM) and with 20 g of urea/kg of DM (35.7 g of N/kg of DM) in a split-plot design. Net flux measurements were made immediately before and after a 72-h mesenteric vein infusion of L-arginine (15 mmol/h). There were no treatment effects on PDV or hepatic O2 consumption. Dietary urea had no effect on splanchnic metabolism of glucose or L-lactate, but arginine infusion decreased net hepatic removal of L-lactate when urea was fed (P < 0.01). Net PDV appearance of n-butyrate was increased by arginine infusion (P < 0.07), and both dietary urea (P < 0.09) and arginine infusion (P < 0.05) increased net hepatic removal of n-butyrate. Dietary urea also increased total splanchnic acetate output (P < 0.06), tended to increase arterial glucagon concentration (P < 0.11), and decreased arterial ST concentration (P < 0.03). Arginine infusion increased arterial concentration (P < 0.07) and net PDV release (P < 0.10) and tended to increase hepatic removal (P < 0.11) of insulin, as well as arterial concentration (P < 0.01) and total splanchnic output (P < 0.01) of glucagon. Despite changes in splanchnic N metabolism, increased ammonia and arginine absorption had little measurable effect on splanchnic metabolism of glucose and other nonnitrogenous components of splanchnic energy metabolism. 相似文献
18.
Subclinical ammonia toxicity in steers: effects on hepatic and portal-drained visceral flux of metabolites and regulatory hormones 总被引：2，自引：0，他引：2
Four calves (avg wt 161 kg) were surgically fitted with indwelling catheters in the femoral artery and femoral, portal, hepatic and mesenteric veins to study the effects of subclinical ammonia toxicity on portal-drained viscera (PDV) and hepatic (HEP) net flux of key metabolites and pancreatic hormones. Hyperammonemia was induced via administration of ammonium chloride (NH4Cl; 12 mumol.kg BW-1.min-1) via the femoral vein catheter for 240 min; infusions were preceded (PRE) and followed (POST) by 60- and 180-min control periods, respectively. Blood samples were obtained from the arterial catheters, and portal and hepatic vein catheters. Net flux rates were calculated by multiplying venoarterial differences by blood flow. Arterial plasma ammonia N peaked (P less than .01) at 327 micrograms/dl; hepatic ammonia extraction increased (P less than .01) from 10 to 23% during NH4Cl infusion. Arterial plasma glucose concentrations increased (P less than .05) during NH4Cl infusion (90.5 vs 82.6 mg/dl) concomitant with trends toward a reduction in net HEP glucose output. Portal-drained visceral release of insulin did not increase (P greater than .10) during NH4Cl infusion despite the steady rise in circulating glucose concentration; however, cessation of NH4Cl infusion resulted in a 109% increase (P less than .05) in PDV insulin release at +60 min POST. Plasma L-lactate, nonesterified fatty acids, urea N and glucagon concentrations and net fluxes were variable throughout the experiment. Results tend to indicate that hyperammonemia reduced hepatic glucose output and glucose-mediated pancreatic insulin release. 相似文献
19.
Six Holstein steers (mean +/- SE BW = 344 +/- 10 kg) fitted with hepatic, portal, and mesenteric vein and mesenteric artery catheters and a ruminal cannula were used in a 6 x 6 Latin square design to evaluate the effects of increasing ruminal butyrate on net portal-drained visceral and hepatic nutrient flux. Steers were fed a 40% brome hay, 60% concentrate diet in 12 portions daily at 1.25 x NEm. Water (control) or butyrate at 50, 100, 150, 200, or 250 mmol/h was supplied continuously via the ruminal cannula. Simultaneous arterial, portal, and hepatic blood samples were taken at hourly intervals from 15 to 20 h of ruminal infusion. Portal and hepatic blood flow was determined by continuous infusion of P-aminohippurate, and net nutrient flux was calculated as the difference between venous and arterial concentrations times blood flow. Ruminal and arterial concentrations and total splanchnic flux of butyrate increased (P less than .01) with increased butyrate infusion. Arterial concentrations of acetate (P less than .10), alpha-amino-N (P less than .05), and glucose (P less than .01) decreased with increased butyrate, whereas arterial beta-hydroxybutyrate (P less than .01) and acetoacetate (P less than .05) increased. Increased butyrate produced an increased portal-drained visceral flux of acetoacetate and an increased net hepatic flux of beta-hydroxybutyrate. Urea N and glucose net portal and hepatic fluxes were not affected by ruminal butyrate. Alpha-amino-N uptake by the liver decreased with increased butyrate (P less than .10). Simple linear regression (r2 = .985) indicated that 25.8% of ruminally infused butyrate appeared in portal blood as butyrate. Only 14% could be accounted for as net portal-drained visceral flux of acetoacetate plus beta-hydroxybutyrate. 相似文献