McLeod K R, Bauer M L, Harmon D L, Reynolds C K, Mitchell G E
Department of Animal Sciences, University of Kentucky, Lexington 40546-0215, USA.
J Anim Sci. 1997 Nov;75(11):3026-37. doi: 10.2527/1997.75113026x.
We used eight Polypay wethers (36 +/- .6 kg BW) fitted with hepatic portal, hepatic venous, mesenteric arterial and venous, and duodenal catheters in a crossover design experiment to determine the influence of somatostatin (SRIF) on splanchnic metabolism. Each crossover period consisted of 14 d, with net flux of nutrients and hormones (venoarterial differences x blood flow) measured on d 14. Before flux measurements, wethers received an i.v. dose (0 h) of either 0 (vehicle) or 50 mg x kg BW(-1) x 10 min(-1) cysteamine (CSH, SRIF-depleting agent) followed by a continuous duodenal infusion (h 10 to 22) of a starch hydrolysate-casein solution. Six sets of arterial, portal, and hepatic blood samples were obtained (h 12 to 16), after which a primed (10 microg), continuous jugular infusion of SRIF-14 (5.0 microg x kg BW(-1) x h(-1)) was initiated and sampling protocol repeated (h 18 to 22). Cysteamine administration increased (P < .01, vs control) portal and hepatic blood flow in the absence of exogenous SRIF (CSH x SRIF, P < .01). Net portal-drained viscera (PDV) release of glucose, alpha-amino N, ammonia N, beta-hydroxybutyrate, and oxygen consumption were decreased (P < or = .10) and lactate release increased (P = .005) during SRIF infusion. The CSH increased (P < .05) PDV release of beta-hydroxybutyrate and insulin and increased (P = .09, CSH alone vs control) net release of glucose in the absence of exogenous SRIF. Exogenous SRIF increased (P = .10) and CSH decreased (P = .09) net hepatic glucose output, whereas liver oxygen consumption was decreased (P = .04) with exogenous SRIF and increased (P = .01) with CSH. Net total splanchnic alpha-amino N release and oxygen consumption were decreased (P < .10) with exogenous SRIF, but CSH increased (P < .05) insulin release and oxygen consumption. These data provide initial evidence for a regulatory involvement of SRIF in visceral metabolism in ruminants.
我们使用了八只波利佩伊阉羊(体重36±0.6千克),在交叉设计实验中给它们安装了肝门静脉、肝静脉、肠系膜动脉和静脉以及十二指肠导管,以确定生长抑素(SRIF)对内脏代谢的影响。每个交叉期为14天,在第14天测量营养物质和激素的净通量(动静脉差值×血流量)。在通量测量前,阉羊静脉注射一剂(0小时)0(赋形剂)或50毫克/千克体重×10分钟⁻¹的半胱胺(CSH,生长抑素耗竭剂),随后在十二指肠持续输注(10至22小时)淀粉水解物-酪蛋白溶液。在12至16小时采集六组动脉、门静脉和肝血样本,之后开始颈静脉首剂(10微克)、持续输注SRIF-14(5.0微克/千克体重×小时⁻¹),并重复采样方案(18至22小时)。在没有外源性SRIF的情况下,给予半胱胺可增加(P<0.01,与对照组相比)门静脉和肝血流量(CSH×SRIF,P<0.01)。在输注SRIF期间,门静脉引流内脏(PDV)的葡萄糖、α-氨基氮、氨氮、β-羟基丁酸盐释放和氧消耗减少(P≤0.10),乳酸释放增加(P=0.005)。在没有外源性SRIF的情况下,CSH增加(P<0.05)PDV的β-羟基丁酸盐和胰岛素释放,并增加(P=0.09,单独使用CSH与对照组相比)葡萄糖的净释放。外源性SRIF增加(P=0.10),CSH减少(P=0.09)肝脏葡萄糖净输出,而外源性SRIF使肝脏氧消耗减少(P=0.04),CSH使其增加(P=0.01)。外源性SRIF使总内脏α-氨基氮净释放和氧消耗减少(P<0.10),但CSH增加(P<0.05)胰岛素释放和氧消耗。这些数据为生长抑素参与反刍动物内脏代谢调节提供了初步证据。