Donmoyer Christine M, Lacy D Brooks, Zhang Yiqun, Chen Sheng-Song, McGuinness Owen P
Department of Molecular Physiology and Biophysics, Vanderbilt University School of Medicine, Nashville, TN 37232-0615, USA.
Am J Physiol Endocrinol Metab. 2002 Dec;283(6):E1151-8. doi: 10.1152/ajpendo.00223.2001.
During chronic total parenteral nutrition (TPN), net hepatic glucose uptake (NHGU) is markedly elevated. However, NHGU is reduced by the presence of an infection. We recently demonstrated that a small, acute (3-h) intraportal fructose infusion can correct the infection-induced impairment in NHGU. The aim of this study was to determine whether the addition of fructose to the TPN persistently enhances NHGU in the presence of an infection. TPN was infused continuously into the inferior vena cava of chronically catheterized dogs for 5 days. On day 3, a bacterial clot was implanted in the peritoneal cavity, and either saline (CON, n = 5) or fructose (+FRUC, 1.0 mg. kg(-1). min(-1), n = 6) infusion was included with the TPN. Forty-two hours after the infection was induced, hepatic glucose metabolism was assessed in conscious dogs with arteriovenous and tracer methods. Arterial plasma glucose concentration was lower with chronic fructose infusion (120 +/- 4 vs. 131 +/- 3 mg/dl, +FRUC vs. CON, P < 0.05); however, NHGU was not enhanced (2.2 +/- 0.5 vs. 2.8 +/- 0.4 mg. kg(-1). min(-1)). Acute removal of the fructose infusion dramatically decreased NHGU (2.2 +/- 0.5 to -0.2 +/- 0.5 mg. kg(-1). min(-1)), and net hepatic lactate release also fell (1.6 +/- 0.3 to 0.5 +/- 0.3 mg. kg(-1). min(-1)). This led to an increase in the arterial plasma glucose (Delta13 +/- 3 mg/dl, P < 0.05) and insulin (Delta5 +/- 2 micro U/ml) concentrations and to a decrease in glucagon (Delta-11 +/- 3 pg/ml) concentration. In conclusion, the addition of chronic fructose infusion to TPN during infection does not lead to a persistent augmentation of NHGU.
在长期全胃肠外营养（TPN）期间，肝脏葡萄糖净摄取量（NHGU）显著升高。然而，感染会降低NHGU。我们最近证明，一次小剂量的急性（3小时）门静脉内输注果糖可纠正感染引起的NHGU损害。本研究的目的是确定在存在感染的情况下，向TPN中添加果糖是否能持续增强NHGU。将TPN连续输注到长期插管犬的下腔静脉中5天。在第3天，将细菌凝块植入腹腔，TPN中加入生理盐水（CON，n = 5）或果糖（+FRUC，1.0 mg·kg⁻¹·min⁻¹，n = 6）输注。感染诱导后42小时，采用动静脉和示踪方法评估清醒犬的肝脏葡萄糖代谢。长期输注果糖后动脉血浆葡萄糖浓度较低（120±4 vs. 131±3 mg/dl，+FRUC vs. CON，P < 0.05）；然而，NHGU并未增强（2.2±0.5 vs. 2.8±0.4 mg·kg⁻¹·min⁻¹）。急性停止输注果糖会显著降低NHGU（2.2±0.5至-0.2±0.5 mg·kg⁻¹·min⁻¹），肝脏乳酸净释放量也下降（1.6±0.3至�0.5±0.3 mg·kg⁻¹·min⁻¹）。这导致动脉血浆葡萄糖（Δ13±3 mg/dl，P < 0.05）和胰岛素（Δ5±2 μU/ml）浓度升高，胰高血糖素（Δ-11±3 pg/ml）浓度降低。总之，在感染期间向TPN中添加长期果糖输注不会导致NHGU持续增加。
