论文部分内容阅读
腺苷酸活化蛋白激酶(AMP activated protein kinase,AMPK)是一种广泛参与多种代谢调节的激酶,是主要的细胞“能量感受器”。AMPK通过α亚基的Thr172发生磷酸化而激活,通过抑制脂质合成相关转录因子以及肝脏糖异生来控制脂质合成以及血糖稳定。肝脏糖异生的调控过程中,通过激素及转录因子如Fox O1、CREB、TORC2、HNF-4α、PGC-1α等的参与,最后将信号传达至糖异生的2个关键性限速酶基因PECK与G6Pase,起到调控作用。激活的AMPK能抑制糖异生转录因子及相关关键酶的有效表达,阻止肝脏发生糖异生,进而下降血糖浓度。本文旨在讨论与总结AMPK在肝脏糖脂代谢中的作用,重点分析AMPK与肝脏糖异生信号通路转录因子之间的联系。
AMP activated protein kinase (AMPK) is a kinase involved in many metabolic regulation and is the main cell “energy receptor ”. AMPK is activated by phosphorylation of Thr172 in the α subunit, and controls lipid synthesis and blood sugar stability by inhibiting lipid synthesis-related transcription factors and liver gluconeogenesis. During the regulation of gluconeogenesis in the liver, through the participation of hormones and transcription factors such as FoxO1, CREB, TORC2, HNF-4α, PGC-1α and so on, the signal is finally transmitted to two key rate-limiting enzyme genes PECK and G6Pase play a regulatory role. Activated AMPK can inhibit the effective expression of gluconeogenesis transcription factor and related key enzymes to prevent the occurrence of gluconeogenesis in the liver, and then lower blood glucose levels. This article aims to discuss and summarize the role of AMPK in liver glucose and lipid metabolism, with emphasis on the relationship between AMPK and hepatic gluconeogenesis signaling transcription factor.