Glucagon-Induced Acetylation of Energy-Sensing Factors in Control of Hepatic Metabolism
Glucagon-Induced Acetylation of Energy-Sensing Factors in Control of Hepatic Metabolism
复制标题
DOI：
10.3390/ijms20081885
复制
发表时间：
2019-04
影响因子：
5.6
通讯作者：
Li Zhang;Weilei Yao;Jun Xia;Tongxin Wang;Feiruo Huang
中科院分区：
文献类型：
--
作者：
Li Zhang;Weilei Yao;Jun Xia;Tongxin Wang;Feiruo Huang
肝脏是糖脂代谢的中枢器官，在生理条件发生变化时调节脂质和葡萄糖的代谢，维持能量稳态。研究人员以前主要关注胰高血糖素磷酸化在控制肝脏代谢中的作用。值得注意的是，新出现的证据表明，胰高血糖素还可以诱导乙酰化，以控制不同生理状态下的肝脏代谢。胰高血糖素通过诱导复杂代谢网络的乙酰化，与多种能量感应因子广泛相互作用，在长时间禁食期间由糖代谢向脂代谢转变。此外，胰高血糖素诱导的不同能量感应因子的乙酰化参与了非酒精性脂肪性肝病（NAFLD）向肝癌的进展。本文就胰高血糖素通过诱导能量敏感因子乙酰化来控制肝脏代谢的最新研究进展进行综述。最后，我们总结并讨论了胰高血糖素在肝脏疾病治疗中的潜在影响。
The liver is the central organ of glycolipid metabolism, which regulates the metabolism of lipids and glucose to maintain energy homeostasis upon alterations of physiological conditions. Researchers formerly focused on the phosphorylation of glucagon in controlling liver metabolism. Noteworthily, emerging evidence has shown glucagon could additionally induce acetylation to control hepatic metabolism in response to different physiological states. Through inducing acetylation of complex metabolic networks, glucagon interacts extensively with various energy-sensing factors in shifting from glucose metabolism to lipid metabolism during prolonged fasting. In addition, glucagon-induced acetylation of different energy-sensing factors is involved in the advancement of nonalcoholic fatty liver disease (NAFLD) to liver cancer. Here, we summarize the latest findings on glucagon to control hepatic metabolism by inducing acetylation of energy-sensing factors. Finally, we summarize and discuss the potential impact of glucagon on the treatment of liver diseases.