Pozefsky T, Felig P, Tobin J D, Soeldner J S, Cahill G F
J Clin Invest. 1969 Dec;48(12):2273-82. doi: 10.1172/JCI106193.
Amino acid balance across skeletal muscle and across subcutaneous adipose tissue plus skin of the forearm has been quantified in postabsorptive man before and after insulin infusion into the brachial artery. Skeletal muscle released significant amounts of alpha amino nitrogen after an overnight fast. Most individual amino acids were released. Alanine output was by far the greatest. The pattern of release probably reflects both the composition of muscle protein undergoing degradation and de novo synthesis of alanine by transamination. A significant correlation was observed between the extent of release of each amino acid and its ambient arterial concentration. Elevation of forearm insulin in eight subjects from postabsorptive (12 muU/ml) to high physiologic levels (157 muU/ml) in addition to stimulating muscle glucose uptake blocked muscle alpha amino nitrogen release by 74%. Consistent declines in output were seen for leucine, isoleucine, tyrosine, phenylalanine, threonine, glycine, and alpha-aminobutyric acid. Alanine output was insignificantly affected. Doubling forearm insulin levels (from 10 to 20 muU/ml) in eight subjects increased muscle glucose uptake in three and blocked alpha amino nitrogen output in two although both effects were seen concurrently in only one subject. Changes in net amino acid balance after insulin could be accounted for by increased transport of amino acids into muscle cells or retardation of their exit. It is likely that ambient arterial amino acid concentrations are established and maintained primarily by the extent of muscle amino acid release. The individual amino acids whose outputs from forearm muscle decline after forearm insulinization correspond well with those whose levels fall systematically after systemic insulinization. This suggests that declines in amino acid levels after systemic insulinization are due to inhibition of muscle release. Doubling basal insulin approaches the threshold both for blockade of muscle amino acid output and stimulation of glucose uptake, effects which appear to occur independently.
在向肱动脉输注胰岛素前后,对处于吸收后状态的男性前臂骨骼肌以及皮下脂肪组织加皮肤的氨基酸平衡进行了定量分析。在禁食过夜后,骨骼肌释放出大量的α-氨基氮。大多数单个氨基酸都有释放。丙氨酸的输出量是最大的。这种释放模式可能既反映了正在降解的肌肉蛋白质的组成,也反映了通过转氨作用从头合成丙氨酸的情况。观察到每种氨基酸的释放程度与其周围动脉浓度之间存在显著相关性。在八名受试者中,将前臂胰岛素水平从吸收后状态(12微单位/毫升)提高到高生理水平(157微单位/毫升),除了刺激肌肉摄取葡萄糖外,还使肌肉α-氨基氮的释放减少了74%。亮氨酸、异亮氨酸、酪氨酸、苯丙氨酸、苏氨酸、甘氨酸和α-氨基丁酸的输出量持续下降。丙氨酸的输出受到的影响不显著。在八名受试者中,将前臂胰岛素水平加倍(从10微单位/毫升提高到20微单位/毫升),有三名受试者的肌肉葡萄糖摄取增加,有两名受试者的α-氨基氮输出受阻,不过只有一名受试者同时出现了这两种效应。胰岛素作用后净氨基酸平衡的变化可能是由于氨基酸向肌肉细胞内转运增加或其外流受阻所致。周围动脉氨基酸浓度很可能主要由肌肉氨基酸的释放程度来确定和维持。前臂胰岛素化后前臂肌肉输出量下降的单个氨基酸,与全身胰岛素化后其水平系统性下降的氨基酸非常吻合。这表明全身胰岛素化后氨基酸水平的下降是由于肌肉释放受到抑制。将基础胰岛素水平加倍接近了阻断肌肉氨基酸输出和刺激葡萄糖摄取的阈值,这两种效应似乎是独立发生的。