Dietze G, Wicklmayr M, Grunst J, Stiegler S, Mehert H
Int Z Vitam Ernahrungsforsch Beih. 1976;15:31-43.
Hepatic metabolic balances derived from arterio-hepatic-venous substrate differences and hepatic blood flow exhibited similar results during fructose infusion (10 g/5 min., 0.5 g/kg x h) as compared to those from the isolated perfused organ: a portion of 55% of splanchnic fructose uptake was accountable for splanchnic glucose production, 25% for splanchnic lactate and pyruvate production and 20% for glycogen - of fat - synthesis and endoxidation. In account of this hepatic metabolism of fructose, glucose homeostasis and insulin secretion almost maintained. However, the small insulin response did not reduce hepatic free fatty acid utilization to such an extent as to increase pyruvate oxidation. Accordingly, splanchnic production of lactate and pyruvate, descending from fructose was enhanced. Since hepatic-venous lactate: pyruvate substrate ratios did not change, the rise of the arterial redox couple could not be due to hepatic fructose metabolism. According to the findings from the isolated perfused organ, fructose seemed to be phosphorylated at a rate which was found to be 2 to 3-fold that of glucose as calculated from splanchnic utilization rates. This high rate of fructose uptake was reduced with increasing insulin levels. The rapid ATP breakdown was followed by an increment of splanchnic oxygen consumption. The larger energy demand seemed to be satisfied by an enhanced endoxidation of free fatty acids. Since diabetics failed to increase their insulin production, their hepatic fructose phosphorylation rate and consequently their hepatic oxygen demand were not limited. Preliminary results concerning metabolic balances from the human forearm during a steady state of fructose supply, underline the notion that fructose has some effects on intermediary metabolism of skeletal muscle. Accordingly, in juvenile diabetics an enhancement of glucose-, lactate- and pyruvate-uptake could be demonstrated.
与离体灌注器官的结果相比,在输注果糖期间(10克/5分钟,0.5克/千克×小时),由肝动静脉底物差异和肝血流量得出的肝脏代谢平衡呈现出相似的结果:内脏果糖摄取的55%部分可解释内脏葡萄糖生成,25%用于内脏乳酸和丙酮酸生成,20%用于糖原 - 脂肪 - 合成及氧化。考虑到果糖的这种肝脏代谢,葡萄糖稳态和胰岛素分泌几乎得以维持。然而,较小的胰岛素反应并未将肝脏游离脂肪酸利用降低到足以增加丙酮酸氧化的程度。因此,果糖来源的内脏乳酸和丙酮酸生成增加。由于肝静脉乳酸:丙酮酸底物比率未改变,动脉氧化还原对的升高不可能归因于肝脏果糖代谢。根据离体灌注器官的研究结果,果糖似乎以一定速率磷酸化,根据内脏利用率计算,该速率是葡萄糖的2至3倍。随着胰岛素水平升高,这种高果糖摄取率降低。快速的ATP分解之后是内脏氧消耗增加。似乎通过增强游离脂肪酸的氧化来满足更大的能量需求。由于糖尿病患者未能增加胰岛素分泌,他们的肝脏果糖磷酸化速率以及因此他们的肝脏氧需求不受限制。在果糖供应稳定状态下人体前臂代谢平衡的初步结果强调了果糖对骨骼肌中间代谢有一些影响的观点。因此,在青少年糖尿病患者中,可以证明葡萄糖、乳酸和丙酮酸摄取增加。