Kilberg M S, Neuhaus O W
J Supramol Struct. 1977;6(2):191-204. doi: 10.1002/jss.400060205.
The transport of 2-aminoisobutyric acid (AIB) into liver tissue was increased by both insulin and glucagon. We have now shown that these hormones do not stimulate the same transport system. Glucagon, possibly via cAMP, increased the hepatic uptake of AIB by a mechanism which resembled system A. This glucagon-sensitive system could be monitored by the use of the model amino acid MeAIB. In contrast, the insulin-stimulated system exhibited little or no affinity for MeAIB and will be referred to as system B. On the basis of other reports that the hepatic transport of AIB is almost entirely Na+ dependent and the present finding that the uptake of 2-aminobicyclo [2,2]heptane-2-carboxylic acid (BCH) was not stimulated by either hormone, we conclude that system B is Na+ dependent. Furthermore, insulin added to the perfusate of livers from glucagon-pretreated donors suppressed the increase in AIB or MeAIB uptake. Depending upon the specificities of systems A and B, both of which are unknown for liver tissue, the insulin/glucagon ratio may alter the composition of the intracellular pool of amino acids.
胰岛素和胰高血糖素均可增加2-氨基异丁酸(AIB)向肝组织的转运。我们现已表明,这些激素刺激的并非同一转运系统。胰高血糖素可能通过环磷酸腺苷(cAMP),通过一种类似于A系统的机制增加肝脏对AIB的摄取。这种对胰高血糖素敏感的系统可用模型氨基酸α-甲基异丁酸(MeAIB)进行监测。相比之下,胰岛素刺激的系统对MeAIB几乎没有亲和力,将其称为B系统。基于其他关于AIB肝脏转运几乎完全依赖钠离子的报道以及目前2-氨基双环[2,2]庚烷-2-羧酸(BCH)摄取不受任何一种激素刺激的发现,我们得出结论,B系统依赖钠离子。此外,向来自经胰高血糖素预处理供体的肝脏灌注液中添加胰岛素会抑制AIB或MeAIB摄取的增加。根据A系统和B系统的特异性(两者对肝脏组织均未知),胰岛素/胰高血糖素比值可能会改变细胞内氨基酸池的组成。