Gersing Sarah, Hansen Torben, Lindorff-Larsen Kresten, Hartmann-Petersen Rasmus
Linderstrøm-Lang Centre for Protein Science, Department of Biology, University of Copenhagen, Ole Maaløes Vej 5, Copenhagen, Denmark.
Novo Nordisk Foundation Center for Basic Metabolic Research, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark.
Trends Biochem Sci. 2025 Mar;50(3):255-266. doi: 10.1016/j.tibs.2024.12.007. Epub 2025 Jan 2.
Human glucokinase (GCK) functions as a glucose sensor in the pancreas and liver, where GCK activity regulates insulin secretion and glycogen synthesis, respectively. GCK's low affinity for glucose and the sigmoidal substrate dependency of enzymatic turnover enables it to act as a sensor that makes cells responsive to changes in circulating glucose levels. Its unusual kinetic properties are intrinsically linked to the enzyme's conformational dynamics. Accordingly, genetic variants that alter the dynamics or other aspects of GCK function are linked to three glucose homeostasis diseases. In this review, we describe the enzyme GCK, focusing on its role as a glucose sensor, its unusual kinetic properties, and recent large-scale efforts to assess GCK variant effects.
人葡萄糖激酶(GCK)在胰腺和肝脏中作为葡萄糖传感器发挥作用,在胰腺中GCK活性分别调节胰岛素分泌,在肝脏中调节糖原合成。GCK对葡萄糖的低亲和力以及酶促周转的S形底物依赖性使其能够作为一种传感器,使细胞对循环葡萄糖水平的变化做出反应。其不寻常的动力学特性与酶的构象动力学内在相关。因此,改变GCK功能动力学或其他方面的基因变异与三种葡萄糖稳态疾病相关。在本综述中,我们描述了GCK酶,重点关注其作为葡萄糖传感器的作用、其不寻常的动力学特性以及最近评估GCK变异效应的大规模研究。