Arnold W C, Holliday M A
Am J Clin Nutr. 1980 Jul;33(7):1428-32. doi: 10.1093/ajcn/33.7.1428.
Resistance to insulin-mediated glucose uptake is well documented in uremia. We have previously reported that in vivo resistance to insulin mediated amino acid uptake is present in the skeletal muscle of acutely uremic rats. This report compares the effect of insulin on in vitro 14C alpha-amino isobutyric acid and cycloleucine uptake by skeletal muscle from uremic and control rats. Intracellular accumulation of 14C alpha-amino isobutyric acid were normal in the diaphragm and epitrochlear muscle of acutely uremic rats in the absence of insulin. However, insulin failed to further stimulate amino acid uptake in both tissues. Insulin also failed to stimulate cellular uptake of cycloleucine in skeletal muscle from acutely uremic animals. Resistance to insulin-mediated amino acid uptake was evident in rats with chronic uremia. This resistance to insulin mediated increases in intracellular amino acid concentration may contribute to the abnormal depression in protein synthesis or the exaggerated gluconeogenesis and alanine turnover seen in uremia.
胰岛素介导的葡萄糖摄取抵抗在尿毒症中已有充分记录。我们之前报道过，急性尿毒症大鼠的骨骼肌中存在对胰岛素介导的氨基酸摄取的体内抵抗。本报告比较了胰岛素对尿毒症大鼠和对照大鼠骨骼肌体外摄取14Cα-氨基异丁酸和环亮氨酸的影响。在无胰岛素的情况下，急性尿毒症大鼠的膈肌和肱三头肌中14Cα-氨基异丁酸的细胞内积累正常。然而，胰岛素未能进一步刺激这两种组织中的氨基酸摄取。胰岛素也未能刺激急性尿毒症动物骨骼肌中环亮氨酸的细胞摄取。慢性尿毒症大鼠中存在对胰岛素介导的氨基酸摄取的抵抗。这种对胰岛素介导的细胞内氨基酸浓度升高的抵抗可能导致尿毒症中蛋白质合成异常降低或糖异生和丙氨酸周转过度。
