Galassetti P, Chu C A, Neal D W, Reed G W, Wasserman D H, Cherrington A D
Department of Molecular Physiology and Biophysics, Vanderbilt University, Nashville, Tennessee 37232-0615, USA.
Am J Physiol. 1999 Jul;277(1):E126-34. doi: 10.1152/ajpendo.1999.277.1.E126.
We investigated whether a negative arterial-portal venous (a-pv) glucose gradient, or "portal signal," can increase net hepatic glucose uptake (NHGU) and decrease muscle glucose uptake at euglycemia as it does at hyperglycemia. Twenty 42-h fasted dogs were studied during a basal and two 120-min euglycemic periods (period I and period II). Glucagon was maintained at basal levels, and insulin was raised 3-fold (3xIns, n = 10) or 15-fold (15xIns, n = 10). During period I, dogs received glucose only peripherally. During period II, one-half of the dogs continued the peripheral infusion; the other one-half received glucose intraportally (4 mg. kg(-1). min(-1) and reduced peripheral glucose infusion). A negative a-pv glucose gradient was present during intraportal glucose infusion. All 3xIns and 15xIns dogs had similar NHGU in period I. In period II, it was 2.1 +/- 0.3 (3xIns) and 2.5 (15xIns) mg. kg(-1). min(-1) greater in the presence than in the absence of the portal signal (P < 0.001). The net glucose fractional extraction data paralleled NHGU. In 3xIns, but not in 15xIns, whole body nonhepatic glucose uptake was lower in the presence of the portal signal than in its absence. In conclusion, in hyperinsulinemic, but not hyperglycemic conditions, the portal signal is effective in activating NHGU. The inhibition of nonhepatic glucose uptake, on the other hand, is minimal under euglycemic as opposed to hyperglycemic conditions.
我们研究了负性动脉-门静脉（a-pv）葡萄糖梯度，即“门静脉信号”，在正常血糖状态下是否能像在高血糖状态时那样增加肝脏葡萄糖净摄取（NHGU）并减少肌肉葡萄糖摄取。对20只禁食42小时的犬在基础状态以及两个120分钟的正常血糖期（I期和II期）进行了研究。胰高血糖素维持在基础水平，胰岛素升高3倍（3xIns，n = 10）或15倍（15xIns，n = 10）。在I期，犬仅经外周输注葡萄糖。在II期，一半的犬继续外周输注；另一半经门静脉输注葡萄糖（4 mg·kg⁻¹·min⁻¹并减少外周葡萄糖输注）。门静脉输注葡萄糖期间存在负性a-pv葡萄糖梯度。所有3xIns和15xIns犬在I期的NHGU相似。在II期，存在门静脉信号时的NHGU比不存在时高2.1±0.3（3xIns）和2.5（15xIns）mg·kg⁻¹·min⁻¹（P < 0.001）。葡萄糖净分数提取数据与NHGU平行。在3xIns组而非15xIns组，存在门静脉信号时全身非肝脏葡萄糖摄取低于不存在时。总之，在高胰岛素血症而非高血糖状态下，门静脉信号可有效激活NHGU。另一方面，与高血糖状态相反，在正常血糖状态下非肝脏葡萄糖摄取的抑制作用最小。
