Hsieh P S, Moore M C, Neal D W, Cherrington A D
Department of Molecular Physiology and Biophysics, Vanderbilt University School of Medicine, Nashville, Tennessee 37232, USA.
Am J Physiol Endocrinol Metab. 2000 Aug;279(2):E284-92. doi: 10.1152/ajpendo.2000.279.2.E284.
The aim of this study was to determine whether the elimination of the hepatic arterial-portal (A-P) venous glucose gradient would alter the effects of portal glucose delivery on hepatic or peripheral glucose uptake. Three groups of 42-h-fasted conscious dogs (n = 7/group) were studied. After a 40-min basal period, somatostatin was infused peripherally along with intraportal insulin (7.2 pmol x kg(-1) x min(-1)) and glucagon (0.65 ng x kg(-1) x min(-1)). In test period 1 (90 min), glucose was infused into a peripheral vein to double the hepatic glucose load (HGL) in all groups. In test period 2 (90 min) of the control group (CONT), saline was infused intraportally; in the other two groups, glucose was infused intraportally (22.2 micromol x kg(-1) x min(-1)). In the second group (PD), saline was simultaneously infused into the hepatic artery; in the third group (PD+HAD), glucose was infused into the hepatic artery to eliminate the negative hepatic A-P glucose gradient. HGL was twofold basal in each test period. Net hepatic glucose uptake (NHGU) was 10.1 +/- 2.2 and 12.8 +/- 2.1 vs. 11.5 +/- 1.6 and 23.8 +/- 3.3* vs. 9.0 +/- 2.4 and 13.8 +/- 4.2 micromol x kg(-1) x min(-1) in the two periods of CONT, PD, and PD+HAD, respectively (* P < 0.05 vs. same test period in PD and PD+HAD). NHGU was 28.9 +/- 1.2 and 39.5 +/- 4.3 vs. 26.3 +/- 3.7 and 24.5 +/- 3.7* vs. 36.1 +/- 3.8 and 53.3 +/- 8.5 micromol x kg(-1) x min(-1) in the first and second periods of CONT, PD, and PD+HAD, respectively (* P < 0.05 vs. same test period in PD and PD+HAD). Thus the increment in NHGU and decrement in extrahepatic glucose uptake caused by the portal signal were significantly reduced by hepatic arterial glucose infusion. These results suggest that the hepatic arterial glucose level plays an important role in generation of the effect of portal glucose delivery on glucose uptake by liver and muscle.
本研究的目的是确定消除肝动脉-门静脉（A-P）葡萄糖梯度是否会改变门静脉葡萄糖输注对肝脏或外周葡萄糖摄取的影响。对三组禁食42小时的清醒犬（每组n = 7）进行了研究。在40分钟的基础期后，外周输注生长抑素，同时门静脉内输注胰岛素（7.2 pmol·kg⁻¹·min⁻¹）和胰高血糖素（0.65 ng·kg⁻¹·min⁻¹）。在试验期1（90分钟），向所有组的外周静脉输注葡萄糖，使肝脏葡萄糖负荷（HGL）加倍。在对照组（CONT）的试验期2（90分钟），门静脉内输注生理盐水；在另外两组中，门静脉内输注葡萄糖（22.2 μmol·kg⁻¹·min⁻¹）。在第二组（PD）中，同时向肝动脉输注生理盐水；在第三组（PD + HAD）中，向肝动脉输注葡萄糖以消除肝A-P葡萄糖负梯度。每个试验期的HGL均为基础值的两倍。对照组（CONT）、PD组和PD + HAD组在两个时期内的净肝脏葡萄糖摄取（NHGU）分别为10.1±2.2和12.8±2.1、11.5±1.6和23.8±3.3*、9.0±2.4和13.8±4.2 μmol·kg⁻¹·min⁻¹（与PD组和PD + HAD组的同一试验期相比，P < 0.05）。CONT组、PD组和PD + HAD组在第一和第二时期内的NHGU分别为28.9±1.2和39.5±4.3、26.3±3.7和24.5±3.7、36.1±3.8和53.3±8.5 μmol·kg⁻¹·min⁻¹（*与PD组和PD + HAD组的同一试验期相比，P < 0.05）。因此，肝动脉输注葡萄糖显著降低了门静脉信号引起的NHGU增加和肝外葡萄糖摄取减少。这些结果表明，肝动脉葡萄糖水平在门静脉葡萄糖输注对肝脏和肌肉葡萄糖摄取的影响产生中起重要作用。
