Fischer C P, Bode B P, Abcouwer S F, Lukaszewicz G C, Souba W W
Shock. 1995 May;3(5):315-22.
Catabolic illness such as sepsis and injury induce profound changes in host amino acid metabolism, including increased hepatic amino acid uptake. Because many amino acid-dependent pathways such as gluconeogenesis and acute-phase protein synthesis are activated in the liver during severe infection, this review will focus on the control of hepatic plasma membrane amino acid transport by specific inflammatory mediators. We specifically review the role of cytokines, eicosanoids, and glucorticoids in this response. Collectively, these signaling molecules act in a concerted manner to exert local control of hepatic function including the stimulation of amino acid transport. In particular, we review the role of glutamine and its transport in the liver, as it occupies a unique role in interorgan ammonia metabolism during critical illness.
分解代谢性疾病，如败血症和损伤，会引起宿主氨基酸代谢的深刻变化，包括肝脏对氨基酸摄取的增加。由于在严重感染期间，肝脏中许多依赖氨基酸的途径，如糖异生和急性期蛋白合成会被激活，因此本综述将聚焦于特定炎症介质对肝细胞膜氨基酸转运的调控。我们将特别综述细胞因子、类花生酸和糖皮质激素在这一反应中的作用。总体而言，这些信号分子协同作用，对肝功能进行局部调控，包括刺激氨基酸转运。特别是，我们将综述谷氨酰胺及其在肝脏中的转运作用，因为它在危重病期间的器官间氨代谢中具有独特作用。
