Institute of Biochemistry Computational Systems Biochemistry Group, Charité - Universitätsmedizin Berlin, Charitéplatz, 110117, Berlin, Germany.
German Federal Institute for Risk Assessment Max-Dohrn-Straße 8-10, 10589, Berlin, Germany.
Nat Commun. 2018 Jun 19;9(1):2386. doi: 10.1038/s41467-018-04720-9.
The epidemic increase of non-alcoholic fatty liver diseases (NAFLD) requires a deeper understanding of the regulatory circuits controlling the response of liver metabolism to nutritional challenges, medical drugs, and genetic enzyme variants. As in vivo studies of human liver metabolism are encumbered with serious ethical and technical issues, we developed a comprehensive biochemistry-based kinetic model of the central liver metabolism including the regulation of enzyme activities by their reactants, allosteric effectors, and hormone-dependent phosphorylation. The utility of the model for basic research and applications in medicine and pharmacology is illustrated by simulating diurnal variations of the metabolic state of the liver at various perturbations caused by nutritional challenges (alcohol), drugs (valproate), and inherited enzyme disorders (galactosemia). Using proteomics data to scale maximal enzyme activities, the model is used to highlight differences in the metabolic functions of normal hepatocytes and malignant liver cells (adenoma and hepatocellular carcinoma).
非酒精性脂肪性肝病 (NAFLD) 的流行增加要求我们更深入地了解控制肝脏代谢对营养挑战、药物和遗传酶变体反应的调节回路。由于人体肝脏代谢的体内研究受到严重的伦理和技术问题的限制,我们开发了一个综合的基于生物化学的中央肝脏代谢动力学模型,包括酶活性受其反应物、变构效应物和激素依赖性磷酸化的调节。该模型通过模拟营养挑战(酒精)、药物(丙戊酸)和遗传酶紊乱(半乳糖血症)引起的各种扰动下肝脏代谢状态的昼夜变化,说明了其在基础研究和医学及药理学中的应用。利用蛋白质组学数据对最大酶活性进行定标,该模型用于突出正常肝细胞和恶性肝细胞(腺瘤和肝癌)的代谢功能差异。