Dietze G, Wicklmayr M, Hepp K D, Bogner W, Mehnert H, Czempiel H, Henftling H G
Diabetologia. 1976 Dec;12(6):555-61. doi: 10.1007/BF01220631.
In 8 subjects in whom portal vein catheters had been inserted 5-6 days previously during cholecystectomy, arterial and portal concentrations of glucose, lactate, pyruvate, glycerol, alanine, free fatty acids, beta-hydroxybutyrate and acetoacetate revealed no significant differences. This provided the basis for the calculation of hepatic balances from arterio-hepatic venous substrate-differences in 17 healthy volunteers. In eight of them metabolic balances were determined during elevated hepatic lactate supply. Kinetics of the substrates throughout the whole test period in 9 controls showed no gross interference from the catheterization or infusion procedure. The elevated hepatic lactate concentration caused a doubling of hepatic glucose output, which could almost entirely be accounted for by a fivefold increase of hepatic lactate uptake. This acceleration of hepatic gluconeogenesis was accompanied by a significant increment of hepatic free fatty acid uptake, whereas hepatic ketone body production did not change. These data seem to support the view that hepatic energy requirements caused by an accelerated gluconeogenesis might be covered from enhanced free fatty acid oxidation.
在8名在胆囊切除术期间5 - 6天前已插入门静脉导管的受试者中，葡萄糖、乳酸、丙酮酸、甘油、丙氨酸、游离脂肪酸、β - 羟基丁酸和乙酰乙酸的动脉血和门静脉血浓度未显示出显著差异。这为根据17名健康志愿者的肝动脉 - 肝静脉底物差异计算肝脏平衡提供了依据。其中8名志愿者在肝脏乳酸供应增加期间测定了代谢平衡。9名对照者在整个测试期间底物的动力学未显示出插管或输注过程的明显干扰。肝脏乳酸浓度升高导致肝脏葡萄糖输出增加一倍，这几乎完全可由肝脏乳酸摄取增加五倍来解释。肝脏糖异生的这种加速伴随着肝脏游离脂肪酸摄取的显著增加，而肝脏酮体生成没有变化。这些数据似乎支持这样一种观点，即加速糖异生所引起的肝脏能量需求可能由增强的游离脂肪酸氧化来满足。
