Effect of a selective rise in hepatic artery insulin on hepatic glucose production in the conscious dog.
Effect of a selective rise in hepatic artery insulin on hepatic glucose production in the conscious dog.
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肝动脉胰岛素选择性升高对清醒狗肝葡萄糖产生的影响。
DOI：
10.1152/ajpendo.1999.276.4.e806
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发表时间：
1999
期刊：
影响因子：
--
通讯作者：
Cherrington,AD
中科院分区：
文献类型：
--
作者：
Sindelar,DK;Igawa,K;Chu,CA;Balcom,JH;Neal,DW;Cherrington,AD
在本研究中，我们比较了肝动脉输注胰岛素引起的肝窦胰岛素选择性增加与门静脉输注胰岛素引起的肝窦胰岛素选择性增加的肝脏效应。用胰钳控制清醒禁食犬的胰腺内分泌。对照组通过外周静脉和门静脉输注胰岛素。基础期40 min后，进入180 min的试验期，在此期间停止外周胰岛素输注，并向肝动脉（HART,n= 5）或门静脉（PORT,n= 5，数据已发表）再输注1.2 pmol⋅kg−1⋅min−1胰岛素。HART组计算肝窦胰岛素水平从99±20（基础）增加到165±21 pmol/l（最后30分钟）。计算肝动脉胰岛素浓度从50±8（基础）上升到289±19 pmol/l（最后30min）。然而，在整个实验过程中，动脉胰岛素水平（50±8 pmol/l）和门静脉胰岛素水平（118±24 pmol/l）没有变化。PORT组计算肝窦胰岛素水平从94±30（基础）增加到156±33 pmol/l（最后30分钟）。门静脉胰岛素从108±42（基础）上升到192±42 pmol/l（最后30分钟），而总体动脉胰岛素（54±6 pmol/l）在研究期间没有变化。两组肝窦胰高血糖素水平保持不变，外周葡萄糖输注维持血糖正常。HART组肝净葡萄糖输出（NHGO）由9.6±2.1 μmol⋅kg−1⋅min−1（基础）抑制至4.6±1.0 μmol⋅kg−1⋅min−1(15 min)，最终降至3.5±0.8 μmol⋅kg−1⋅min−1（最后30 min，P< 0.05）。PORT组NHGO快速下降（P< 0.05），从10.0±0.9（基础）下降到7.8±1.6 (15 min)，最终达到3.1±1.1 μmol⋅kg−1⋅min−1（最后30 min）。因此，NHGO会随着肝窦胰岛素的选择性增加而减少，无论这是由于肝动脉或门静脉的高胰岛素血症引起的。
In the present study we compared the hepatic effects of a selective increase in hepatic sinusoidal insulin brought about by insulin infusion into the hepatic artery with those resulting from insulin infusion into the portal vein. A pancreatic clamp was used to control the endocrine pancreas in conscious overnight-fasted dogs. In the control period, insulin was infused via peripheral vein and the portal vein. After the 40-min basal period, there was a 180-min test period during which the peripheral insulin infusion was stopped and an additional 1.2 pmol ⋅ kg−1⋅ min−1of insulin was infused into the hepatic artery (HART,n= 5) or the portal vein (PORT,n= 5, data published previously). In the HART group, the calculated hepatic sinusoidal insulin level increased from 99 ± 20 (basal) to 165 ± 21 pmol/l (last 30 min). The calculated hepatic artery insulin concentration rose from 50 ± 8 (basal) to 289 ± 19 pmol/l (last 30 min). However, the overall arterial (50 ± 8 pmol/l) and portal vein insulin levels (118 ± 24 pmol/l) did not change over the course of the experiment. In the PORT group, the calculated hepatic sinusoidal insulin level increased from 94 ± 30 (basal) to 156 ± 33 pmol/l (last 30 min). The portal insulin rose from 108 ± 42 (basal) to 192 ± 42 pmol/l (last 30 min), whereas the overall arterial insulin (54 ± 6 pmol/l) was unaltered during the study. In both groups hepatic sinusoidal glucagon levels remained unchanged, and euglycemia was maintained by peripheral glucose infusion. In the HART group, net hepatic glucose output (NHGO) was suppressed from 9.6 ± 2.1 μmol ⋅ kg−1⋅ min−1(basal) to 4.6 ± 1.0 μmol ⋅ kg−1⋅ min−1(15 min) and eventually fell to 3.5 ± 0.8 μmol ⋅ kg−1⋅ min−1(last 30 min,P< 0.05). In the PORT group, NHGO dropped quickly (P< 0.05) from 10.0 ± 0.9 (basal) to 7.8 ± 1.6 (15 min) and eventually reached 3.1 ± 1.1 μmol ⋅ kg−1⋅ min−1(last 30 min). Thus NHGO decreases in response to a selective increase in hepatic sinusoidal insulin, regardless of whether it comes about because of hyperinsulinemia in the hepatic artery or portal vein.
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