CENEXA, Centro de Endocrinología Experimental y Aplicada (UNLP-CONICET LA PLATA, Centro Colaborador OPS/OMS), Facultad de Ciencias Médicas, 60 y 120, 1900 La Plata, Argentina.
IUBMB Life. 2011 Jan;63(1):1-6. doi: 10.1002/iub.411. Epub 2011 Jan 13.
Blood glucose is the primary cellular substrate and in vivo must be tightly maintained. The liver plays a key role in glucose homeostasis increasing or decreasing glucose output and uptake during fasting and feeding. Glucokinase (GCK) is central to this process. Its activity is modulated in a coordinated manner via a complex set of mechanisms: in the postprandial period, the simultaneous rise in glucose and insulin increases GCK activity by enhanced gene expression, changes in cellular location, and interaction with regulatory proteins. Conversely, in the fasting state, the combined decrease in glucose and insulin concentrations and increase in glucagon concentrations, halt GCK activity. Herein we summarize the current knowledge regarding the regulation of hepatic GCK activity.
血糖是细胞的主要底物,在体内必须被严格维持。肝脏在葡萄糖稳态中起着关键作用,在禁食和进食期间增加或减少葡萄糖的输出和摄取。葡萄糖激酶(GCK)是这一过程的核心。其活性通过一系列复杂的机制以协调的方式进行调节:在餐后期间,葡萄糖和胰岛素的同时升高通过增强基因表达、细胞位置的变化以及与调节蛋白的相互作用来增加 GCK 活性。相反,在禁食状态下,葡萄糖和胰岛素浓度的联合下降以及胰高血糖素浓度的升高,会抑制 GCK 活性。本文总结了目前关于肝 GCK 活性调节的知识。