McGuinness O P, Donmoyer C, Ejiofor J, McElligott S, Lacy D B
Department of Molecular Physiology and Biophysics, Vanderbilt University School of Medicine, Nashville, TN 37232-0615, USA.
Am J Physiol. 1998 Nov;275(5):E763-9. doi: 10.1152/ajpendo.1998.275.5.E763.
We examined the impact of infection on hepatic and muscle glucose metabolism in dogs adapted to chronic total parenteral nutrition (TPN). Studies were done in five conscious chronically catheterized dogs, in which sampling (artery, portal and hepatic vein, and iliac vein), infusion catheters (inferior vena cava), and Transonic flow probes (hepatic artery, portal vein, and iliac artery) were implanted. Fourteen days after surgery, dogs were placed on TPN. After 5 days of TPN, an infection was induced, and the TPN was continued. The balance of substrates across the liver and limb was assessed on the day before infection (day 0) and 18 (day 1) and 42 h (day 2) after infection. On day 0, the liver was a marked net consumer of glucose (4.3 +/- 0.6 mg. kg-1. min-1) despite near normoglycemia (117 +/- 5 mg/dl) and only mild hyperinsulinemia (16 +/- 2 microU/ml). In addition, the majority (79 +/- 13%) of the glucose taken up by the liver was released as lactate (34 +/- 6 micromol. kg-1. min-1). After infection, net hepatic glucose uptake decreased markedly on day 1 (1.6 +/- 0.9 mg. kg-1. min-1) and remained suppressed on day 2 (2.4 +/- 0.5 mg. kg-1. min-1). Net hepatic lactate output also decreased on days 1 and 2 (15 +/- 5 and 12 +/- 3 micromol. kg-1. min-1, respectively). This occurred despite increases in arterial plasma glucose on days 1 and 2 (135 +/- 9 and 144 +/- 9 mg/dl, respectively) and insulin levels on days 1 and 2 (57 +/- 14 and 34 +/- 9 microU/ml, respectively). In summary, the liver undergoes a profound adaptation to TPN, making it a major site of glucose disposal and conversion to lactate. Infection impairs hepatic glucose uptake, forcing TPN-derived glucose to be removed by peripheral tissues.
我们研究了感染对适应慢性全胃肠外营养（TPN）的犬肝脏和肌肉葡萄糖代谢的影响。对五只清醒的长期留置导管的犬进行了研究，在这些犬身上植入了采样导管（动脉、门静脉、肝静脉和髂静脉）、输液导管（下腔静脉）以及Transonic血流探头（肝动脉、门静脉和髂动脉）。手术后14天，给犬实施TPN。TPN治疗5天后，诱发感染，并继续进行TPN治疗。在感染前一天（第0天）以及感染后18小时（第1天）和42小时（第2天）评估肝脏和肢体的底物平衡。在第0天，尽管血糖接近正常（117±5mg/dl）且仅有轻度高胰岛素血症（16±2μU/ml），肝脏仍是显著的葡萄糖净消耗器官（4.3±0.6mg·kg⁻¹·min⁻¹）。此外，肝脏摄取的大部分葡萄糖（79±13%）以乳酸形式释放（34±6μmol·kg⁻¹·min⁻¹）。感染后，肝脏葡萄糖净摄取在第1天显著下降（1.6±0.9mg·kg⁻¹·min⁻¹），并在第2天持续受到抑制（2.4±0.5mg·kg⁻¹·min⁻¹）。肝脏乳酸净输出在第1天和第2天也下降（分别为15±5和12±3μmol·kg⁻¹·min⁻¹）。尽管第1天和第2天动脉血浆葡萄糖水平升高（分别为135±9和144±9mg/dl）以及胰岛素水平升高（分别为57±14和34±9μU/ml），这种情况仍发生。总之，肝脏对TPN会发生深刻的适应性变化，使其成为葡萄糖处置和转化为乳酸的主要场所。感染会损害肝脏对葡萄糖的摄取，迫使TPN来源的葡萄糖被外周组织清除。
