Paul H S, Adibi S A
J Nutr. 1976 Aug;106(8):1079-88. doi: 10.1093/jn/106.8.1079.
The present investigations of rates of oxidation of [U-14C] or [1-14C]leucine by homogenates of gastrocnemius muscle of fed and starved rats have indicated that 14CO2 production is mainly the result of alpha-decarboxylation of leucine in this tissue. This incomplete oxidation was not the result of imparied tricarboxylic acid cycle since the oxidation of palmitate proceeded to completion within the experimental conditions. In the subsequent studies, the effect of altered nutrition and metabolic factors on alpha-decarboxylation of leucine by gastrocnemius muscle homogenates was investigated. Starvation increased the rate of alpha-decarboxylation of leucine. Glucose or palmitate (C16) added in physiological concentrations to the incubation medium were without effect on decarboxylation of leucine, but this reaction was stimulated by addition of 1 mM hexanoate (C6) or octanoate (C8) to the incubation medium. However, when fatty acid chain length was elongated to C10 (decanoate), the stimulatory effect was not only abolished, but this fatty acid significantly inhibited the rate of leucine decarboxylation. Addition of insulin, epinephrine, glucagon and cyclic AMP within a wide range of concentrations to the incubation medium did not significantly affect the rate of decarboxylation of leucine. These studies indicate a complex interrelationship between the metabolism of leucine and that of fatty acids.
目前对喂食和饥饿大鼠腓肠肌匀浆中[U-14C]或[1-14C]亮氨酸氧化速率的研究表明，14CO2 的产生主要是该组织中亮氨酸α-脱羧作用的结果。这种不完全氧化并非三羧酸循环受损所致，因为在实验条件下棕榈酸的氧化进行到了完全。在随后的研究中，研究了营养和代谢因素改变对腓肠肌匀浆中亮氨酸α-脱羧作用的影响。饥饿增加了亮氨酸α-脱羧的速率。向孵育培养基中添加生理浓度的葡萄糖或棕榈酸（C16）对亮氨酸的脱羧作用没有影响，但向孵育培养基中添加 1 mM 己酸（C6）或辛酸（C8）可刺激该反应。然而，当脂肪酸链长度延长至 C10（癸酸）时，刺激作用不仅消失，而且这种脂肪酸显著抑制亮氨酸脱羧的速率。向孵育培养基中添加各种浓度范围内的胰岛素、肾上腺素、胰高血糖素和环磷酸腺苷对亮氨酸脱羧速率没有显著影响。这些研究表明亮氨酸代谢与脂肪酸代谢之间存在复杂的相互关系。
