Ouchi K, Sakai K, Matsubara S, Mikuni J, Katayose Y, Matsuno S
Department of Surgery, Tohoku University School of Medicine, Sendai, Japan.
Nutrition. 1994 Sep-Oct;10(5):411-4.
Clinical studies and experiments in rats were carried out to elucidate changes in fuel utilization after hepatectomy. In addition, the effect of glucose hyperalimentation on energy metabolism in the liver remnant was studied. Respiratory quotient (RQ) and substrate oxidation rate for fat and glucose were evaluated by indirect calorimetry in eight patients who had undergone liver resection. Patients had a reduced nonprotein RQ of approximately 0.85 and a reduced ratio of glucose to fat oxidation of approximately 2.0 on the 1st and 2nd postoperative days. After 80% hepatectomy, rats received either 30 kcal.kg-1.day-1 (group 1) or 200 kcal.kg-1.day-1 (group 2) of glucose for 48 h. In both rat groups, hepatic mitochondrial ATP synthesis 12 and 24 h after hepatectomy was accelerated when palmitic acid was used as the substrate and suppressed when pyruvate was used compared with sham-operated groups. This suggests that the energy substrate of the remnant liver was principally fatty acids rather than glucose, which seems to occur also in humans. Hepatic energy charge was within normal limits in group 1 (0.862 +/- 0.008) but decreased significantly in group 2 (0.818 +/- 0.006, p < 0.01) 12 h after hepatectomy. An abundance of glucose in the early postoperative period therefore caused a hepatic energy derangement by suppressing endogenous fat oxidation. This suppression was corroborated by the findings of lower immunoreactive glucagon and nonesterified fatty acid concentration in group 2. Therefore, glucose hyperalimentation in the early postoperative period after liver resection is not recommended.
开展了临床研究及大鼠实验，以阐明肝切除术后燃料利用的变化。此外，还研究了葡萄糖高营养对肝残余组织能量代谢的影响。通过间接量热法评估了8例肝切除患者的呼吸商（RQ）以及脂肪和葡萄糖的底物氧化率。术后第1天和第2天，患者的非蛋白RQ降低至约0.85，葡萄糖与脂肪氧化的比率降低至约2.0。80%肝切除术后，大鼠接受48小时的葡萄糖输注，剂量分别为30 kcal.kg-1.day-1（第1组）或200 kcal.kg-1.day-1（第2组）。与假手术组相比，在两组大鼠中，肝切除术后12小时和24小时，以棕榈酸为底物时肝线粒体ATP合成加速，而以丙酮酸为底物时则受到抑制。这表明肝残余组织的能量底物主要是脂肪酸而非葡萄糖，这似乎在人类中也会发生。肝能量电荷在第1组（0.862±0.008）处于正常范围内，但在肝切除术后12小时第2组显著降低（0.818±0.006，p<0.01）。因此，术后早期大量葡萄糖通过抑制内源性脂肪氧化导致肝能量紊乱。第2组中较低的免疫反应性胰高血糖素和非酯化脂肪酸浓度的结果证实了这种抑制作用。因此，不建议在肝切除术后早期进行葡萄糖高营养。
